City Hall station (IRT Lexington Avenue Line)

The City Hall station, also known as City Hall Loop, was a terminal station on the IRT Lexington Avenue Line of the New York City Subway. It was under City Hall Park next to New York City Hall in Civic Center, Manhattan. The City Hall station was constructed for the Interborough Rapid Transit Company (IRT) as the southern terminal of the city's first subway line, which was approved in 1900. Construction of the segment of the line that includes the City Hall station started on September 12 of the same year. The station opened on October 27, 1904, as one of the original 28 stations of the New York City Subway. As ridership grew, it was deemed infeasible to lengthen the original 257 ft (78 m) platform to accommodate ten-car trains. The station was closed on December 31, 1945, because of its proximity to the Brooklyn Bridge station.

The City Hall station, with its single track and curved side platform, was the showpiece of the original IRT subway. The single platform and mezzanine feature Guastavino tile, skylights, colored glass tilework, and brass chandeliers. The Rafael Guastavino-designed station is unique in the system for the usage of Romanesque Revival architecture. The tunnel passing through the City Hall station is still used as a turning loop for the and can be seen from passing trains. The station is a New York City designated landmark and listed on the National Register of Historic Places.

## History

### Construction and opening

Planning for a subway line in New York City dates to 1864. However, development of what would become the city's first subway line did not start until 1894, when the New York State Legislature passed the Rapid Transit Act. The subway plans were drawn up by a team of engineers led by William Barclay Parsons, the Rapid Transit Commission's chief engineer. They called for a subway line from New York City Hall in lower Manhattan to the Upper West Side, where two branches would lead north into the Bronx. A plan was formally adopted in 1897, and all legal conflicts concerning the route alignment were resolved near the end of 1899. The Rapid Transit Construction Company, organized by John B. McDonald and funded by August Belmont Jr., signed the initial Contract 1 with the Rapid Transit Commission in February 1900, in which it would construct the subway and maintain a 50-year operating lease from the opening of the line. In 1901, the firm of Heins & LaFarge was hired to design the underground stations. Belmont incorporated the Interborough Rapid Transit Company (IRT) in April 1902 to operate the subway.

The station had always been envisioned as a terminal with loop tracks. The initial plans in the 1890s called for a multi-track loop, extending beneath the City Hall Post Office and Courthouse, which was then at the southern corner of City Hall Park. The loop was planned to have either two tracks (on two levels) or four tracks. When the plans for the IRT line were changed in 1898 to allow the express tracks to go to Brooklyn as part of the subway's Contract 2, the planned City Hall station was changed to a single-track local station, thereby avoiding a grade crossing with the express tracks. Under the 1898 iteration of the plan, the loop was to diverge from the line at the south end of Centre Street, traveling west under City Hall Park, south under Broadway, and then northeast under Park Row. In addition, tracks from the loop would have led to the post office building. East of the loop, there were two express tracks and two storage tracks.

#### Construction of the loop

A formal groundbreaking ceremony was performed at City Hall on March 24, 1900, pursuant to the contract's requirements. The ceremony was officiated by then-Mayor Robert Van Wyck. Degnon-McLean Contracting Company was awarded the contract for Section 1, from the City Hall loop to Chambers Street. Work began promptly after the groundbreaking. The tunnel was built using a cut and cover method, with steel beams supporting a concrete roof made of jack arches. A further change was requested in September 1900, which would provide more room for the loop on the Park Row side. Plans for the loop under City Hall Park were modified in January 1901, providing for a shortened loop. By that March, the City Hall Loop was planned to be built just north of the post office, rather than around it. At the end of the month, trees in City Hall Park were being removed in preparation for the loop's construction.

The portion of the loop in City Hall Park was excavated starting in April 1901. The trees were removed from the park using derricks. One worker was killed that May when a derrick boom in front of the subway excavation was knocked loose. Sand from the 500 ft-long (152 m) excavation was sold to builders who sought the sand for its "good quality". The short section adjacent to the post office could not be constructed because the Treasury Secretary had not approved the work, leading the IRT to request approval from Congress. The entirety of the loop within City Hall Park had been excavated by that August. Most of the excavation was covered over shortly afterward, although a small part remained open to facilitate work on the station.

In late 1901, the contractors began excavating the tunnel under Park Row, which would carry both the northbound track of the loop and the express tracks to Brooklyn. Work on the station was placed on hold because the station's concrete vaults were difficult to pour during winter. By February 1902, three-fourths of the work for the station's side walls had been completed, and work had started on the vaults. The tunnel under Park Row had been fully excavated and was being covered with steel beams. Most of the loop was completed by late 1902, except for the section under the post office. The contractors excavated the remainder of the loop after they were given temporary permission, in December 1902, to use the vaults underneath the post office.

#### Completion

By late 1903, the tilework of the sidewalks and the station's staircase were completed. Construction materials were being stored in the station's only entrance and exit. The subway was nearly complete, but the IRT Powerhouse and the system's electrical substations were still under construction, delaying the system's opening. On New Year's Day 1904, mayor George B. McClellan Jr. and a group of wealthy New Yorkers gathered at the City Hall station and traveled 6 mi (9.7 km) to 125th Street using handcars. The IRT conducted several more handcar trips afterward. The first train to run on its own power traveled from 125th Street to City Hall in April 1904.

The City Hall station opened on October 27, 1904, as the southern terminal station of the original 28-station New York City Subway line to 145th Street on the West Side Branch, now the Broadway–Seventh Avenue Line. At the time, the station was called "City Hall Loop". Prior to the opening, more than 15,000 people were issued passes for the first series of rides from the City Hall station's platform. McClellan attended the opening ceremonies, which began at 1:00 p.m. The first subway train departed from City Hall at precisely 2:34 p.m., with McClellan at the controls. President A. E. Orr of the Rapid Transit Board requested that all New Yorkers join in the celebration by blowing whistles and ringing bells. The new line carried 27,000 passengers for free until 6 p.m., and another 125,000 passengers paid to ride the subway in the six-hour period that followed.

### Operation

#### Early years

Because of the limited number of entrances to the City Hall station, it was served exclusively by local trains, which also stopped at the much larger Brooklyn Bridge station. All express trains terminated at Brooklyn Bridge and did not go around the loop. Furthermore, the City Hall station was originally an entrance-only station; disembarking passengers had to go to the Brooklyn Bridge station. After the Fulton Street station opened in January 1905, the City Hall Loop was served by local trains to the West Side Branch at all times and by local trains to 145th Street on the East Side Branch (now Lenox Avenue Line) during the daytime. By July 1905, East Side local trains to 145th Street ran to City Hall at all times, while West Side locals bypassed this station and went to Bowling Green or South Ferry. To address ventilation issues, the IRT installed ventilation grates in City Hall Park in mid-1906. By the end of the year, West Side locals ran to City Hall during rush hours, and East Side locals ran to City Hall at all times.

Not long after the station opened, the IRT started displaying advertisements in the station, which was highly controversial but was allowed under the IRT's contract to operate the route. The New York City government initially did not find the ads to be problematic, but public outcry led the city to file a lawsuit to force the IRT to remove the ads. In 1907, the New York Supreme Court ruled that the IRT was allowed to keep the ads. To address overcrowding, in 1909, the New York Public Service Commission proposed lengthening the platforms at stations along the original IRT subway. As part of a modification to the IRT's construction contracts made on January 18, 1910, the company was to lengthen station platforms to accommodate ten-car express and six-car local trains. The City Hall station was not lengthened, but the platforms at other stations were extended, and six-car local trains began operating in October 1910.

In 1918, the Lexington Avenue Line opened north of Grand Central–42nd Street, and the original line was divided into an "H"-shaped system. All local trains were sent via the Lexington Avenue Line, running along the Pelham Line in the Bronx. In 1938, as part of a remodeling of City Hall Park, city parks commissioner Robert Moses proposed relocating the entrances of the IRT's City Hall station and those of the Brooklyn–Manhattan Transit Corporation (BMT)'s adjacent City Hall station. The city government took over the IRT's operations on June 12, 1940.

#### Decline

Increased subway ridership led to longer trains, and thus longer platforms, in the years after the subway's construction. The City Hall station, built on a tight curve, would have been difficult to lengthen, and it was also quite close to the far busier Brooklyn Bridge–City Hall station. In addition, the new, longer trains had center doors in each car, which were an unsafe distance from the platform edge. Movable platform extensions were installed to fill the gap. By the 1930s, the New York Herald Tribune reported that the City Hall station was little used, "and many of the younger generation have never seen it". During World War II, shortly before the station's closure, the skylights were blacked out with tar for safety.

In its final years, the City Hall station was not open at night and on Sundays, when trains continued to South Ferry. The majority of passengers used the Brooklyn Bridge station, which was only about 600 ft (180 m) away. The Brooklyn Bridge IRT station provided both local and express service, including trains to Brooklyn, and it was much closer to the Brooklyn Bridge streetcar terminal and the BMT's Park Row elevated station. The city also wanted to operate ten-car trains after taking over the IRT, but the City Hall station could only fit six cars. Given the extensive renovations that would have been required to bring the station up to modern standards and the fact that the city wanted to improve City Hall Park by removing the entrance kiosks, the city decided to close the station instead. The final day of service was December 31, 1945. The station recorded 255,000 entries in its final year, or about 800 entries per day. By contrast, the Brooklyn Bridge station had 14 million entries the same year.

### Post-closure

The New York Transit Museum (NYTM) considered the City Hall station as a possible location in 1965. The museum ultimately decided to move to the abandoned Court Street station in Brooklyn. The station occasionally was used for tours after its closure, including in 1979 for an event celebrating the subway's 75th anniversary. In 1979, the New York City Landmarks Preservation Commission designated the City Hall station as a city landmark, along with eleven other stations on the original IRT.

#### Proposals for reuse

By the 1980s, Mayor Ed Koch suggested allowing a restaurant to open in the old station as part of a larger plan to renovate City Hall Park. As part of this plan, replicas of the IRT's original cast-iron entrance kiosks would have been built. Civic leaders and city officials visited the station in July 1986. Ross Sandler, the city's transportation commissioner and a proponent of the station's reopening, lamented that the station was a "designated landmark that people can't visit". The plan had still not advanced over a year later, when parks commissioner Henry J. Stern said the station's restoration was dependent on whether funding to renovate City Hall Park was secured. Ultimately, the idea was overruled by the New York City Police Department, which expressed concerns that the station's location beneath New York City Hall was a security vulnerability.

In April 1995, the NYTM sought funding to reopen the station as a branch of the museum. The New York City Transit Authority (NYCTA) estimated that about \$1 million would be needed just to reopen the station, though the NYTM wished to raise \$3.5 million. The museum had secured a \$750,000 federal grant and a \$350,000 grant from the NYCTA by that November. By 1997, some \$2 million in state and federal funding had been allocated. Had the NYTM branch been built, it would have contained two entrances from street level. Early the next year, MTA officials started refurbishing the station's corridors and offered up to \$5 million for underground repairs to City Hall Park, which at the time was being renovated. However, in late 1998, the administration of mayor Rudy Giuliani rejected the proposal, citing security risks in the area around City Hall after terrorist bombings in Nairobi and Dar es Salaam. Plans for the museum annex were abandoned, and museum tours ceased for several years. The MTA did spend \$2 million to repair structural issues at the City Hall station.

#### 21st century

By 2001, the NYCTA planned to temporarily reopen the station three years later for the subway's 100th anniversary. The station was listed on the National Register of Historic Places in 2004. For the subway's Centennial Celebration the same year, one of the street entrances was restored, and the station was opened for the duration of the celebration. Other than that, the station was used only as an emergency exit. By the mid-2000s, the staff of the Transit Museum were again conducting tours of the station; only NYTM members were allowed on these tours. Unlike other abandoned New York City Subway stations, there was generally little graffiti or dust in the City Hall station. The station remained in good condition in 2019, though only one of the original skylights remained. Due to the COVID-19 pandemic in New York City, the NYTM suspended its tours of the station between 2020 and 2023.

## Station layout

The station consists of a concave 257 ft (78 m)-long side platform along a single balloon loop track, which could fit five cars. The radius of curvature of the track is about 150 ft (46 m), meaning that the platform curves approximately 98.2 degrees between its front and back ends. As a result, when the station was in service, there were significant platform gaps between the train doors and the platform. The center doors of IRT rolling stock were as much as 2 ft (0.61 m) away from the concave platform. The fare control area was on a mezzanine slightly above platform level, connected to the platform by a single, wide staircase. Intended as the showpiece of the entire subway system, the City Hall station was designed in a completely different style from the remaining stations on the IRT subway.

According to the Railroad Gazette, all of the City Hall station's public areas were designed "with a view to the beauty of their appearance, as well as to their efficiency", since the station was "a great public work". One observer wrote that there was "not a straight line" in the entire station when it was completed. The travel magazine Travel + Leisure ranked the station 12th in its list of "the most beautiful subway stations in the world" in November 2009. A replica of the station was built for the feature film Fantastic Beasts And Where To Find Them. In addition, the station may have been the model for the Teenage Mutant Ninja Turtles' lair.

### Design

The station was designed by Rafael Guastavino, and it makes extensive use of classic Guastavino tile to sheathe its soaring roof arches. The main consulting architects were Heins & LaFarge, which designed all of the other IRT stations. This station is unusually elegant in architectural style, and is unique among the original IRT stations, employing Romanesque Revival architecture. The station was constructed by cut-and-cover construction. The bottom of the station shell contains a foundation of concrete no less than 4 in (100 mm) thick. There is a 1 in (25 mm) gap between the trough wall and the station walls, which are made of 4 in (100 mm)-thick brick covered over by a tiled finish.

The ceiling is made of twelve Guastavino vaults. The ceiling surfaces are composed of white tiles, with green and brown tiles along the perimeter of each ceiling vault. The vaults were constructed of thin terracotta tiles bonded with a string mortar, added in successive layers to form a thin structural vault of great strength. Three vaults had leaded glass skylights, which opened upward to vault lights in City Hall Park. The skylights, designed with floral tracery, were blacked out during World War II and were restored in the 2000s. Additional lighting was supplied by twelve chandeliers hung from the center of the vaults, which contain floral motifs and nickel finishes. The chandeliers near the skylights have five arms, while the others have four.

The platform is made of poured concrete. The platforms still contain markings from where the platform extensions were formerly installed. The top half of the wall along the platform, under each of the arches, consists of Roman brick. At the bottom half of each wall is a marble course topped by a brick wainscoting and another marble course. On the platform walls are three blue-on-white faience plaques with letters reading city hall, flanked by a pair of triangles and surrounded by green and buff tiles. Two of these plaques are rectangular, installed on the walls under the brick arches. The third is curved and is installed on an archway above the staircase that leads to the mezzanine. The mosaic tiles at all original IRT stations were manufactured by the American Encaustic Tile Company, which subcontracted the installations at each station. On the trackside wall, facing the platform, are three bronze plaques with the names of important figures involved in the original IRT's construction, including Parsons, McDonald, Belmont, Rapid Transit Subway Construction Company officials, engineering staff, mayors, commissioners, and city comptrollers. Gutzon Borglum designed the plaques.

The walls of the staircase between mezzanine and platform level are covered with yellow, green, and blue tile. The mezzanine contains a vaulted ceiling with a quoin pattern, consisting of brown trim with white and green tiles. The center of the mezzanine has an oculus skylight, with light bulbs around the skylight. The walls of the mezzanine contain large glass tiles interspersed with opaque ceramic tile. Wire conduits and pipes have been installed onto the mezzanine walls. The mezzanine once had an ornamented oak ticket booth, which has since been removed.

### Track layout

North of the City Hall station, the IRT Lexington Avenue Line carries four tracks. From west to east, these are the downtown local track, the downtown express track, the uptown express track, and the uptown local track. The loop connects the downtown and uptown local tracks. The track is slightly canted toward the inner wall of the loop. When the loop was completed, Scientific American magazine wrote that "one of the more important tasks of constrictive engineering which the subway presented is solved".

South of the Brooklyn Bridge station, there is a switch on the downtown local track, allowing trains to leave service and enter either of two storage tracks. Trains in service turn onto a balloon loop, continuing past the abandoned side platform on the west side of the loop, and returning to the Brooklyn Bridge station on the uptown local track. The uptown and downtown express tracks pass above the loop, continuing south.

### Exits and access

There were two staircases from outside the City Hall building to the mezzanine of the station, each measuring 6 ft (1.8 m) wide. Heins & LaFarge designed entrance and exit "kiosks" for the City Hall station and the other underground IRT stations. These structures were extremely ornate structures made of cast iron and glass, being inspired by those on the Budapest Metro, which themselves were inspired by ornate summer houses called "kushks". Brooklyn-based manufacturer Hecla Iron Works manufactured the kiosks. Exit kiosks were distinguished by their four-sided pyramidal wire-glass skylights, while entrance kiosks had domed roofs with cast-iron shingles. The kiosks also carried ventilation shafts for the stations' restrooms, which were generally directly underneath each kiosk. One critic said the station's original entrance and exit kiosks gave "a foreign appearance" to City Hall Park and compared the vaults to the interior of a mosque.

After the City Hall station closed, the staircases were covered with slabs. Since then, the only access point to the City Hall station has been a set of metal cellar doors in the ground. On the surface, all that can be seen is a concrete slab inset with glass tiles, the skylights for the platform below. This patch of concrete is in the middle of a grove of dogwoods in front of City Hall, close to Broadway. At street level, in the pavement in front of City Hall, a plaque commemorates the groundbreaking for the subway in 1900.

The station can be viewed by passengers who stay on the as they travel around the loop to head back uptown. Under MTA policy, all riders on southbound must leave the train at Brooklyn Bridge, but the policy is rarely enforced; by the 2010s, the MTA was intentionally allowing riders to stay on the train. Artificial lighting has often been dimmed to save electricity, but the skylights provide some illumination during the daytime. The loop track is classified as a revenue track, since trains can carry passengers through the loop. The announcement programs on the R142A subway cars, which were formerly used on the , announced that trains would turn around via the loop and stop on the northbound platform at Brooklyn Bridge.

## See also

- List of closed New York City Subway stations
- List of New York City Subway stations in Manhattan
- List of New York City Designated Landmarks in Manhattan below 14th Street
- National Register of Historic Places listings in Manhattan below 14th Street
- Beach Pneumatic Transit, in the basement of the nearby Rogers Peet Building

New York City Subway station, 1904–1945

1945 disestablishments in New York (state)

Defunct Interborough Rapid Transit Company stations

Former elevated and subway stations in Manhattan

Railway and subway stations on the National Register of Historic Places in Manhattan

Railway stations in the United States opened in 1904


1998 FA Cup final

The 1998 FA Cup final was a football match between Arsenal and Newcastle United on 16 May 1998 at the old Wembley Stadium, London. It was the final match of the 1997–98 FA Cup, the 117th season of the world's oldest football knockout competition, the FA Cup. Six-time winners Arsenal were appearing in their thirteenth final, whereas Newcastle United, having also won the competition six times, appeared in their eleventh final. It was the third time both teams faced each other in a FA Cup final; Newcastle won the previous two encounters in 1932 and 1952.

Each team had progressed through five rounds to reach the final. Arsenal's victories were close affairs and the team required three replays, two of which ended in penalty shootouts. Newcastle's progress was more comfortable by comparison and needed only one replay in the fourth round, against Stevenage Borough. Arsenal entered the match as favourites; a fortnight prior the club won the Premier League and aimed to complete the club's second league and cup double.

Watched by a stadium crowd of 79,183 and a British television audience of more than seven million, Arsenal took a first half lead through Marc Overmars. Newcastle's performance improved in the second half, and striker Alan Shearer almost equalised when his shot hit the inside of David Seaman's post. Moments later the league champions extended their lead when Nicolas Anelka was put through to score. Arsenal's victory was heralded by the English press, and the club capped off its memorable season with an open-top bus parade. It was Arsène Wenger's first FA Cup triumph as a coach; he went on to win six more finals in a 22-year spell at the club to become the competition's most successful manager.

## Route to the final

The FA Cup is English football's primary cup competition. Clubs in the Premier League enter the FA Cup in the third round and are drawn randomly out of a hat with the remaining clubs. If a match is drawn, a replay comes into force, ordinarily at the ground of the team who were away for the first game. As with league fixtures, FA Cup matches are subject to change in the event of games being selected for television coverage and this often can be influenced by clashes with other competitions.

### Arsenal

Arsenal entered the competition in the third round, and their opening match was against First Division club Port Vale at Highbury. It ended a goalless draw and the match was replayed at Vale Park. Neither side managed to find a winning goal after normal and extra time, meaning the tie headed into a penalty shoot-out. Arsenal won out 4–3; Allen Tankard missed the decisive penalty kick for Port Vale. In the fourth round, Arsenal played Middlesbrough at the Riverside Stadium. The visitors began strongly as Marc Overmars scored the opener inside 68 seconds, and his teammate Ray Parlour added a second to give Arsenal a commanding lead going into the interval. Although Paul Merson scored in the second half for Middlesbrough and they pushed for an equaliser, Arsenal held out for a 2–1 win.

In the fifth round Arsenal faced Crystal Palace at home, but once again had to settle for a replay as the team were held to a draw. Arsenal fielded a makeshift side at Selhurst Park, but goals from Nicolas Anelka and Dennis Bergkamp ensured progress into the next round. Against West Ham United in the quarter-finals, Arsenal went a goal behind as Frank Lampard's corner kick was converted into the goal net by Ian Pearce. Although Bergkamp equalised from the penalty spot, West Ham defended well enough to force a replay.

At Upton Park, Bergkamp was sent off in the first half for elbowing West Ham captain Steve Lomas in the face. Anelka put Arsenal in front, but John Hartson equalised for the hosts late on. The tie was eventually settled on penalties, which ended 4–3 in Arsenal's favour. A goal by Christopher Wreh against Wolverhampton Wanderers in the semi-final was enough for Arsenal to win the match and reach the final.

### Newcastle United

Newcastle's FA Cup campaign began in the third round against fellow league side Everton. The only goal of the match came in the second half; John Beresford's right-wing cross beat the Everton defence and allowed John Barnes to hook the ball back from beyond the far post. Ian Rush forced the ball over the line, and in the process set a new goalscoring record – scoring 43 goals in the competition. Newcastle were drawn away to non-league Stevenage Borough in the fourth round. Alan Shearer on his return scored inside the first three minutes; he headed the ball into the net after good play from Keith Gillespie. Giuliano Grazioli equalised for the home side and they held on for a replay at St James' Park.

In the rematch, Shearer scored both goals against Stevenage Borough. His manager Kenny Dalglish was irritated at the lack of courtesy his opponents had shown, and said afterwards: "Off the pitch they have a lot to learn about manners. If they were a Premier League club they would probably have been done for bringing the game into disrepute." A 1–0 win in the fifth round at home to Tranmere Rovers was followed by a quarter-final draw against Barnsley, who had knocked out competition favourites Manchester United. Newcastle advanced to the semi-finals after a 3–1 win and at Old Trafford, Shearer scored the winner against Sheffield United.

## Pre-match

Arsenal were appearing in the final of the FA Cup for the first time since 1993. They had won the cup on six separate occasions (in 1930, 1936, 1950, 1971, 1979 and 1993) and lost the showpiece final by the same amount. Newcastle in contrast were making their first Cup final appearance in 24 years. The club had won six FA Cups, and came runners-up five times, most recently against Liverpool in 1974.

The 1998 final marked the third meeting between Arsenal and Newcastle United in Cup final history. Newcastle were victorious on both occasions: the first match in 1932 ended 2–1 in their favour, while the second, staged twenty years later, was a much tighter affair and George Robledo's goal settled the game. The recent head-to-head record between the clubs was vastly different. In Dalglish's first full season at Newcastle, his team struggled for consistency and spent much of the Premier League campaign hovering in mid-table. They lost both matches against Arsenal, 1–0 at home in December 1997 and 3–0 away in April 1998. It marked a turnaround in fortune as Newcastle for the past two seasons had competed intensely with Manchester United for the league title. Arsenal on the other hand hit their stride in the final months of the season. The team, managed by Arsène Wenger, had made up a sizable gap on Manchester United to win the title. In doing so, Wenger became the first non-British manager to win the league championship in England.

Arsenal were favourites to win the FA Cup, and on course to complete a "unlikely" double. The fitness of Bergkamp, who was instrumental in Arsenal's successful season, was a major story in the days leading up to the final. The striker had limped out of their game against Derby County in late April, and after it emerged he pulled his hamstring Bergkamp was ruled out for the remainder of Arsenal's league campaign. Wenger revealed two days before the final that Bergkamp had resumed training and "medically he looked all right", but the player received a further setback when he suffered a reaction to his hamstring. He ruled himself out of the match and told reporters: "I'm very disappointed. As a little boy in Holland I always watched the FA Cup final. And I used to dream about playing in it myself one day." Ian Wright was listed as Bergkamp's probable replacement to partner Anelka.

Newcastle had their own issues surrounding Shearer. The England international was involved in a tangle with Leicester City player Neil Lennon during a league match, which went unnoticed by the referee. Television cameras showed Shearer kicking Lennon in the face, something he denied was premeditated. He was charged with misconduct, but escaped a ban from the FA's disciplinary panel. Shearer's teammate Rob Lee felt the striker was in the right shape of mind to face Arsenal, saying: "He's too strong a person to have let that affect him, even if it hadn't been sorted." Dalglish talked before the game of Newcastle's disappointing league campaign and questioned "why we couldn't translate our Cup results into the league". He dismissed talk of Newcastle having an "easy run" in the competition, saying "It's not our fault if our opponents beat teams who were favourites to go through."

Continuing a tradition which began in the 1970s, the finalists each released a song as part of the buildup to the final. The Arsenal squad recorded a cover of Donna Summer's "Hot Stuff" with proceeds going to the Arsenal Charitable Trust, while Newcastle enlisted celebrity supporter Sting to write "Black and White Army (Bringing the Pride Back Home)". Arsenal's song spent seven weeks in the UK Singles Chart and peaked at number nine. Royalty was present at Wembley on the day of the final; Prince Edward, Duke of Kent was on hand to perform various duties alongside his wife Katharine, Duchess of Kent. Players from both sides were adorned in Hugo Boss suits for their customary pre-match walk.

## Match

### Summary

Wenger selected Wreh to lead Arsenal's attack, and left Wright on the substitutes’ bench. The Liberian striker partnered Anelka in a front two, and they were supported by wide midfielders Overmars and Parlour. Dalglish named Alessandro Pistone in the starting eleven to play as right back; commentator John Motson suggested the defender's role was to nullify Overmars. Temuri Ketsbaia was picked ahead of Andreas Andersson and John Barnes started the game on the bench. Rush did not make the 16-man squad for Newcastle, as he failed to recover from injury. Both clubs were set up in a traditional 4–4–2 system: a four-man defence (comprising two centre-backs and left and right full-backs), four midfielders (two in the centre, and one on each wing) and two centre-forwards.

Newcastle kicked-off the final on a warm Saturday afternoon and quickly set about testing Arsenal by aiming long balls in their half. Arsenal won many of the aerial duels and broke quickly once they had possession. Parlour chased after a long ball by Dixon from the right, but Howey impeded the midfielder and put the ball out for a corner. It came to nothing as the whistle was blown once Adams's climbed above his opponent. Newcastle's first attempt on goal was created by Ketsbaia, who won the ball near the centre of the pitch. He shifted it onto his left foot, but his shot from about 20 yards (18 m) bobbled past Arsenal goalkeeper David Seaman's left-hand post. Arsenal's first real chance was a move which began from the backline. Vieira found Parlour who kicked the ball towards Dixon. The Arsenal right-back saw Parlour making a dart forward into the opposition's penalty area and returned the ball to the midfielder. Parlour's cross from the right was met by Anelka in the box, but the striker headed the ball over the post. Arsenal took the lead minutes later through Overmars. A through-ball by Emmanuel Petit had found the charging winger and he resisted the challenge of Pistone to prod the ball through the legs of the onrushing goalkeeper Shay Given. It was Overmars' 16th goal of the campaign, his most prolific season as a professional footballer. Newcastle struggled to breach Arsenal's stable defence for the remainder of the first half; Ketsbaia saw his curling shot on target but comfortably caught by Seaman. Overmars, a constant threat in the match, crossed the ball towards Parlour in the penalty area, but with room to shoot the midfielder skied it over. Newcastle appealed for a penalty deep into added time after Adams jumped over Shearer while looking to clear the ball, but the referee immediately turned it down.

In the second half, Newcastle began more adventurously and forced Arsenal into moving the ball at a higher tempo. From a free-kick awarded near the left channel, Lee crossed the ball and up rose Nikos Dabizas, whose header hit the bar. Newcastle were presented with another opportunity to equalise after Arsenal defender Martin Keown slipped on the ball. Shearer pounced, but his left-foot shot hit the foot of the post, and rebounded back out. Newcastle were punished for poor finishing in the 69th minute as Anelka scored for Arsenal. Parlour lifted the ball through to the teenage striker who controlled it with his chest. He raced past his marker Dabizas, and steered the ball into the bottom left-hand corner. Newcastle responded by bringing on Andersson, an extra forward, in place of Pearce but the change in personnel made no difference to the outcome. Parlour, later awarded man of the match, nearly scored a third for Arsenal, but his effort hit the side netting. As the whistle blew for full-time, Wenger hugged his assistant Pat Rice in the dugout before joining his players on the field for celebrations. Sportingly, the Newcastle fans applauded the Arsenal team as they made their way up the Wembley steps to collect the trophy.

### Details

### Statistics

## Post-match

Arsenal's win had sealed a league and cup double and Wenger, the club's manager, described it as "the greatest moment of my sporting life." Speaking to the media, he complimented his team for their performance and said of the season: "We kept getting better and so has the mixture between the foreign and English players." Wenger reserved praise for the goalscorers Overmars ("a world-class player") and Anelka ("Nicolas is very young. But you saw in the second half today what he can do"), and felt the turning point in the match was Shearer's shot hitting the post. He sympathised with Newcastle, as did his captain, Adams who said afterwards: "The team and their fans did everything they could out there, but it was our day. It capped a fantastic season for us and was a day we'll never forget." Overmars called winning the FA Cup, "...the biggest thing that you can dream of. I'd say it's the same as winning the European Cup", while Dixon, a long-serving member of the team, added Arsenal's achievement had "...surpasse[d] anything that we've done in the past."

Dalglish congratulated Arsenal on completing the double, as well as both sets of supporters: "I think it's the first time I've come to Wembley and seen both sets of fans applauding the winning side." He felt Newcastle's performance improved in the second half – "...our players seemed to have more belief in themselves", though concluded despite the efforts it "just wasn't to be." Pearce agreed with his manager that Arsenal deserved the win and told reporters: "We failed to deliver and our magnificent fans deserved better. We'll have to come back stronger next season."

Journalists and pundits reviewing the final unanimously agreed that Arsenal were deserved winners. Ian Ridley wrote in The Independent on Sunday of 17 May 1998: "Where Arsenal played legato, Newcastle were staccato in their passing and though they enjoyed a purple patch after raising the tempo in the second half, twice hitting the goal frame, they were largely limp opposition." The Guardian football correspondent David Lacey was in awe of the double winners' performance, writing "There have been more distinguished Wembley triumphs but it is hard to remember a final being won with the sheet pace of Arsenal's victory over Newcastle on Saturday." Paul Wilson of The Observer believed in comparison to their title charge it was "lukewarm stuff", while The Sunday Times match reporter Joe Lovejoy felt the London club had got the better of Newcastle in what was a "pretty ordinary game". Lovejoy did however credit the Newcastle support – "The Toon Army won the decibel count, which was no surprise." David Pleat wrote in his analysis column for The Sunday Times that key to Arsenal's victory was winning the midfield battle. He singled the "prodigious" Parlour out for praise, writing "nobody did more efficient work than the man rejuvenated at Arsenal."

The match was broadcast live in the United Kingdom by both ITV and Sky Sports; the former provided the free-to-air coverage and Sky Sports 2 was the pay-TV alternative. Highlights were also shown on Match of the Day that evening on BBC One. ITV held the majority of the viewership, with an overnight audience of 7.8 million viewers (65% viewing share), whereas 900,000 watched on Sky. The terrestrial figure was the lowest in Cup final history in more than a decade, which ITV attributed to the May heatwave.

A day after the win Arsenal paraded both trophies on an open-top bus, heading towards Islington Town Hall for a civic reception. The club's victory set up a Charity Shield match against Manchester United, the league runners-up, in August 1998. As cup winners, Arsenal would have ordinarily been awarded a spot in the UEFA Cup Winners' Cup, but as the club qualified for the UEFA Champions League via their league position the place was passed to finalists Newcastle United.

## Aftermath and legacy

Arsenal were unable to retain the FA Cup the following season as the team fell to Manchester United at the semi-final stage. It was not until 2001 that they appeared in another Cup final, where Michael Owen scored twice at Cardiff's Millennium Stadium to hand Liverpool the trophy. Arsenal regrouped the following year, starting a run of three FA Cup wins in four years. By 2015, Wenger had led Arsenal to a record-breaking 13th FA Cup and victory against Chelsea in 2017 earnt him the accolade of being the most successful manager in the competition's history.

The 1998 Cup final was the climax to an eventful season for Wenger, who became the first manager born outside of the British Isles to complete the double. As well as revitalising the club, his style of management was heralded as revolutionary. Rob Hughes in his Times column of 18 May 1998 credited the Arsenal manager for demonstrating "what there is to learn from overseas", and for blending players of different ages and cultural backgrounds into a successful squad. The 1998 double-winning team is regarded as one of English football's finest; former Manchester United winger Ryan Giggs later described them as one of his toughest opponents: "They just had a bit of everything really. Quality with Bergkamp, pace with Anelka and Overmars, the experience of the back four, and then the toughness of Vieira and Petit in midfield."

For Newcastle, success was hard to come by. In August 1998, just two matches into the Premier League season, Dalglish was dismissed, replaced by former Chelsea manager Ruud Gullit. Although the team reached another FA Cup final in 1999, they were again losing finalists.

Association football championship match between Arsenal and Newcastle United, held in 1998

May 1998 sports events in the United Kingdom


Dominant white

Dominant white (W) is a group of genetically related coat color alleles on the KIT gene of the horse, best known for producing an all-white coat, but also able to produce various forms of white spotting, as well as bold white markings. Prior to the discovery of the W allelic series, many of these patterns were described by the term sabino, which is still used by some breed registries.

White-colored horses are born with unpigmented pink skin and white hair, usually with dark eyes. Under normal conditions, at least one parent must be dominant white to produce dominant white offspring. However, most of the currently-known alleles can be linked to a documented spontaneous mutation that began with a single ancestor born of non-dominant white parents. Horses that exhibit white spotting will have pink skin under the white markings, but usually have dark skin beneath any dark hair.

There are many different alleles that produce dominant white or white spotting; as of 2022 they are labeled W1 through W28 and W30 through W35, plus the first W allele discovered was named Sabino 1 (SB-1) instead of W1. They are associated with the KIT gene. The white spotting produced can range from white markings like those made by W20, to the irregularly-shaped or roaning patterns previously described as Sabino, to a fully white or almost fully white horse.

For many of the W alleles, the white coats are, as the name suggests, inherited dominantly, meaning that a horse only needs one copy of the allele to have a white or white spotted coat. In fact, some such alleles may be embryonic lethal when homozygous. Others, such as SB-1 and W20, are incomplete dominants, capable of producing viable offspring with two copies of the gene, and who generally have more white than horses with only one copy. In addition, different alleles which on their own give a white-spotted but not completely white horse, such as W5 and W10, can combine to make a horse completely white.

White can occur in any breed, and has been studied in many different breeds. Because of the wide range of patterns produced, some suggest the family be called “white spotting” rather than “white.” Other researchers suggest the term "dominant white" be used only for the W alleles thought to be embryonic lethal when homozygous.

White is both genetically and visually distinct from gray and cremello. Dominant white is not the same as lethal white syndrome, nor are white horses "albinos"—Tyrosinase negative albinism has never been documented in horses.

## Description

Although the term "dominant white" is typically associated with a pure white coat, such horses may be all-white, near-white, partially white, or exhibit an irregular spotting pattern similar to that of sabino horses. To add to the confusion, at least some horses in each of those groups might be referred to as "dominant white", "white spotted", or "sabino". The amount of white hair depends on which KIT alleles are involved. At birth, most of the white hair is rooted in unpigmented pink skin. The pink skin lacks melanocytes, and appears pink from the underlying network of capillaries. White spotting is not known to affect eye color, and most white horses have brown eyes.

### White or near-white

White horses are born with pink skin and a white coat, which they retain throughout their lives. The genetic factors that produce an all-white horse are often also capable of producing a near-white horse, which is mostly white but has some areas that are pigmented normally. Near-white horses most commonly have color in the hair and skin along the topline (dorsal midline) of the horse, in the mane, and on the ears. The color is often interspersed as specks or spots on a white background. In addition, the hooves are usually white, but may have striping if there is pigmented skin on the coronary band just above the hoof. In some cases, foals born with residual non-white hair may lose some or all of this pigment with age, without the help of the gray factor.

### White spotting

White spotting from a W allele is difficult to identify visually, as it can range from small white markings in the case of a heterozygous W20 horse all the way to an obvious pinto pattern. In addition, even completely white horses can have genes which by themselves would only give white spotting, such as W20 combined with W22 or W5 combined with W10. As such, the only reliable way to find out whether a horse has one of the known white spotting patterns from an allele on KIT is to have it genetically tested.

## Prevalence

Dominant white is one of several potential genetic causes for horses with near-white or completely white coats; it may occur through spontaneous mutation, and thus may be found unexpectedly in any breed, even those that discourage excessive white markings. To date, forms of dominant white have been identified in Thoroughbreds, Standardbreds, American Quarter Horses, Frederiksborg horses, Icelandic horses, Shetland ponies, Franches Montagnes horses, South German Draft horses, and the Arabian horse. The American White Horse, which is descended primarily from one white stallion crossed on non-white mares, is known for its white coat, as is the Camarillo White Horse.

## Inheritance

The W locus was mapped to the KIT gene in 2007. KIT is short for "KIT proto-oncogene receptor tyrosine kinase". White spotting is caused by multiple forms, or alleles, of the KIT gene. All horses possess the KIT gene, as it is necessary for survival even at the earliest stages of development. The presence or absence of dominant white is based on the presence of certain altered variants of KIT. Each unique form is called an allele, and for every trait, all animals inherit one allele from each parent. The original or "normal" form of KIT, which is expected in horses without dominant white spotting, is called the "wild type" allele. Thus, a dominant white horse has at least one KIT allele with a mutation associated with dominant white spotting.

### Allelic series

The KIT gene contains over 2000 base pairs, and a change in any of those base pairs results in a mutant allele. Over forty seven such alleles have been identified by sequencing the KIT genes of various horses. The resultant phenotype of many of these alleles is not yet known, but over 30 have been linked to white spotting. DNA tests can identify if a horse carries the identified W alleles.

- SB-1 (Sabino 1) was first identified in 2005. The allele was designated with "SB" in an attempt to align with traditional equine coat color terminology. It is located on the KIT gene and is a single nucleotide polymorphism designated KI16+1037A. The mutation results in the skipping of exon 17.When heterozygous, it creates a distinctive white spotting pattern of irregular, rough-edged white patches that usually include two or more white feet or legs, a blaze, spots or roaning on the belly or flanks, and jagged margins to white markings. Homozygous foals are typically at least 90% white-coated at birth, and sometimes termed "Sabino-White."

- W1 was the second KIT allele found to be involved in horse coat color. The researchers who discovered W1-4 decided to name them "W" following the convention in mice, rather than continuing the "SB" series. W1 is found in Franches Montagnes horses descended from a white mare named Cigale born in 1957. Cigale's parents' coats were not extensively marked. A single nucleotide polymorphism (SNP), a type of mutation in which a single nucleotide is accidentally exchanged for another, is thought to have occurred with Cigale. This mutation (c.2151C\>G) is predicted to truncate the protein in the middle of the tyrosine kinase domain, which would severely affect the function of KIT. It is a nonsense mutation located on exon 15 of KIT. Some horses with the W1 mutation are born pure white, but many have residual pigment along the topline, which they may then lose over time. Based on studies of KIT mutations in mice, the severity of this mutation suggests that it may be nonviable in the homozygous state. However, horses with the W1 mutation have been found to have normal blood parameters and do not suffer from anemia.

- W2 is found in Thoroughbred horses descended from KY Colonel, a stallion born in 1946. While KY Colonel was described as a chestnut with extensive white markings, he is known for siring a family of pure white horses through his white daughter, White Beauty, born in 1963. His son War Colors was registered as roan because he had some spots of color, but later became white. The W2 allele is linked to a single nucleotide polymorphism (c.1960G\>A), a missense mutation where a glycine is replaced with arginine (p.G654R) in the protein kinase domain, located on exon 17.
- W3 is found in Arabian horses descended from R Khasper, a near-white stallion born in 1996. Neither of his parents were white, and the causative mutation (c.706A\>T) is thought to have originated with this horse. It is a nonsense mutation on exon 4, predicted to truncate the protein in the extracellular domain. Horses with the W3 allele often retain interspersed flecks or regions of pigmented skin and hair, which may fade with time. Some members of this family possess blue eyes, but these are thought to be inherited separately from the white coat. Based on similar studies in mice, researchers have named W3 as potentially homozygous nonviable.
- W4 is found in Camarillo White Horses, a breed characterized by a white coat, beginning with a spontaneous white stallion born in 1912 named Sultan. Like W1 and W3, these horses may be pure white or near-white, with pigmented areas along the topline that fade with time. This mutation is an SNP (c.1805C\>T) which produces a missense mutation replacing alanine with valine in the kinase domain, on exon 12.

- W5 is found in Thoroughbreds descending from Puchilingui, a 1984 stallion with sabino-like white spotting and roaning. Horses with the W5 allele exhibit a huge range in white phenotype: a few have been pure white or near-white, while others have sabino-like spotting limited to high, irregular stockings and blazes that covered the face. Twenty-two members of this family were studied, and the 12 with some degree of white spotting were found to have a deletion in exon 15 (p.T732QfsX9), in the form of a frameshift mutation. A later study found that the members of this family with the greatest depigmentation were compound heterozygotes who also carried the W20 allele.
- W6 is found in one near-white Thoroughbred named Marumatsu Live born to non-white parents in 2004. The potential range of expressivity, therefore, is not yet known. The mutation (c.856G\>A) is thought to have occurred spontaneously in this horse. It is a missense mutation on exon 5.
- W7 is found in another near-white Thoroughbred named Turf Club born in 2005 to a dam that had nine other offspring, all non-white. The dam did not possess the W7 allele, which results from a splice site mutation (c.338-1G\>C), located on intron 2 of KIT.
- W8 was found in an Icelandic horse with sabino-like white spotting, mottling, and roaning, named Þokkadís vom Rosenhof. Both parents and four maternal half-siblings, all non-white, were found without the W8 allele. The W8 allele is also a splice site mutation (c.2222-1G\>A), located on intron 15.
- W9 was found in an all-white Holsteiner horse with a single nucleotide polymorphism (c.1789G\>A). No relatives were studied, but both parents are non-white. It is a missense mutation on exon 12.
- W10 was found in a study of 27 horses in a family of American Quarter Horses, 10 of which were white or spotted and 17 that were solid and non-white. The 10 family members with W10 had a frameshifting deletion in exon 7 (c.1126_1129delGAAC). Like W5, a wide range of phenotypes were observed. The most modestly marked had large amounts of white on the face and legs and some medium-sized belly spots, while another was nearly all-white. The founder of this line was GQ Santana, foaled in 2000.
- W11 is found in a family of South German Draft Horses descending from a single white stallion, in which the causative mutation is thought to have originated. The stallion is suspected to be Schimmel, foaled in 1997. The mutation responsible for the W11 phenotype is a splice site mutation of intron 20 (c.2684+1G\>A).
- W12 was found in a single Thoroughbred colt, about half white, who both was born and died in 2010. The mutation is a deletion mutation found on exon 3.
- W13 causes a fully white phenotype, and appears to be homozygous lethal. It was first found in a family Quarter Horse and Paso Peruviano crossbreds, and since has been seen in multiple horse and pony breeds, including some not descended from Quarter horse ancestors. The cause is a splice site mutation on intron 17.

- W14 is a deletion mutation on exon 17, found in Thoroughbreds. The founder is suspected to be Shirayukihime, born in 1996. Horses with this mutation are usually fully white but may have some spots of color.
- W15 is found in Arabians, and is a missense mutation on exon 10. The founder is suspected to be Khartoon Khlassic, born in 1996. Horses heterozygous for W15 tend to be partially white, while homozygotes are fully white.
- W16 is found in the Oldenburger and is a missense mutation on exon 18. The three horses studied looked like roany sabinos or near whites, and the founder is suspected to be Celene, born in 2003.
- W17 is found in a Japanese Draft horse and is a pair of missense mutations on exon 14. The horse studied was white with one brown eye and one blue eye.
- W18 is a splice site mutation on intron 8 (c.1346 +1G\>A) found in a bay Swiss Warmblood named Colorina von Hoff, who had extensive speckling. Both parents were solid-colored and had no extended head or leg markings.
- W19 was found in three part-Arabians with bald face markings, white leg markings extending above the knees and hocks, and irregular belly spots. All three horses tested negative for sabino-1, frame overo and splashed white. W19 is a missense mutation on exon 8 (c.1322A.G; p.Tur41Cys). The founder is suspected to be Fantasia Vu, born in 1990. W19 causes a bald face, extensive leg white, and belly spots. One horse has tested as W19/W19, indicating this allele is likely not homozygous lethal. However, all W19/W19 have presented at birth as max white and all that have been tested at maturity have been sterile. In Europe this was confirmed with extensive testing

- W20 is associated with bold face and leg markings, and can greatly increase the amount of white when combined with certain other white patterns. The W20 sequence was first discovered in 2007, but was not recognized for its effect on coat color until 2013. Horses with one copy of W5 or W22 combined with one copy of W20 tend to be white or nearly all white. W20 on its own does tend towards adding white.

W20 has been found in many breeds including the German Riding Pony, German Warmblood, Thoroughbred, Oldenburger, Welsh pony, Quarter horse, Paint horse, Appaloosa, Noriker, Old-Tori, Gypsy horse, Morgan horse, Clydesdale horse, Franches-Montagnes, Marwari horse, South German Draft, Paso Peruano, Camarillo White Horse, and Hanoverian horse.

W20 is a missense mutation on exon 14 (c.2045G\>A; p.Arg682His).

- W21 is a single nucleotide deletion found in Icelandics. The founder is Ellert frá Baldurshaga, who has a mostly white face with speckles and irregular patches of white across his body. The color has been named "ýruskjóttur".
- W22 is a deletion thought to have originated in the Thoroughbred mare Not Quite White, born in 1989. She passed it to her two foals Airdrie Apache and Spotted Lady. On its own, W22 is sabino-like, but when paired with W20, it gives a completely white horse.
- W23 was found in the white Arabian stallion Boomori Simply Stunning, who had two white foals Meadowview Ivory and Just a Dream. However, the line appears to have died out.
- W24 is a mutation that disrupts splicing of KIT. The founder is a white Trottatore Italiano named Via Lattea, born in 2014.
- W25 is a missense mutation on exon 4. The founder is suspected to be the Australian Thoroughbred mare Laughyoumay. She has had one pure white foal with blue eyes, who also carries frame, and one near-white colt with some color on and around the ears.
- W26 is a single base pair deletion suspected to have originated with the Australian Thoroughbred mare Marbrowell, born in 1997.
- W27 is a missense mutation thought to originate with the Australian Thoroughbred mare Milady Fair. Most horses with this mutation are descended from her great-grand-colt, Colorful Gambler, who has an extensive sabino-like pattern.
- W28 is a deletion found in a German Riding Pony.
- W29 has not been assigned.
- W30 is found in a family of Berber horses. It is a missense mutation identical to the second missense mutation in W17. The horses with W30 are white or almost fully white.
- W31 traces to an American Quarter Horse stallion, Cookin Merada. It leads to an early stop on the KIT protein sequence, truncating the protein.
- W32 was found in a family of American Paint Horses, and seems to have a mild effect leading to high white on the limbs, belly spots and white facial markings. It is unclear whether the SNP described is actually the causative mutation, or merely linked to it.
- W33 is a de novo variant found in a Standardbred horse that results in sabino-like white spotting.
- W34 is a missense mutation linked to increased white spotting, found in multiple breeds including the American Paint Horse, American Quarter Horse, Appaloosa, Arabian, Mangalarga, Morgan, Mustang, Rocky Mountain horse and some Warmblood breeds.

- W35 is associated with more white than is usually seen on Quarter horses. Researchers found a mutation in the untranslated region on the 5' side of KIT that correlates with the increased white, but it may only be a nearby marker rather than the actual cause. This variant is also called "Holiday" after the horse in which it was discovered. Some horses are homozygous for the marker.
- Classic Roan is associated with the KIT gene.
- Tobiano is caused by an inversion starting about 100 kb downstream of KIT, and is also considered an allele of KIT.

These alleles do not account for all dominantly inherited white spotting in horses. More KIT alleles are expected to be found with roles in white spotting. Most W alleles occur within a specific breed or family and arise as spontaneous mutations. KIT appears to be prone to mutation, in part due to its many exons, so new alleles of W can occur in any breed. There are likely many KIT variants in the global horse population that have not yet been investigated.

### Relation to sabino

Sabino can refer either specifically to Sabino 1 (SB1) or to a variety of visually similar spotting patterns. SB1 creates a nearly pure white horse when homozygous, and bold spotting when heterozygous. To add to the confusion, white spotting created by several W alleles, such as W5, W15, and W19 creates patterns that historically were called sabino. For that reason, the use of the word "sabino" is evolving. Genetically, Sabino 1 is simply another allele on KIT, and thus can be classified in the same “family” of KIT mutations as the alleles labeled W or dominant white.

In its homozygous form, Sabino 1 can be confused with dominant white alleles such as W1, W2, W3, or W4 that create a white or near-white horse with only one copy. Both dominant white and "Sabino-White" horses are identified by all-white or near-white coats with underlying pink skin and dark eyes, often with residual pigment along the dorsal midline. However, it takes two copies of Sabino 1 to produce a Sabino-white horse, and Sabino 1 is not homozygous lethal.

Initially, dominant white was separated from sabino on the grounds that the former had to be entirely white, while the latter could possess some pigment. However, the 2007 and 2009 studies of dominant white showed that many dominant white alleles produce a range of white phenotypes that include horses with pigmented spots in their hair and skin. Each of the larger families of dominant white studied included pure-white horses, horses described as having "sabino-like" white markings, as well as white horses described as "maximal sabino".

More recently, dominant white and sabino were distinguished from one another on the grounds that dominant white alleles produce nonviable embryos in the homozygous state, while Sabino 1 was viable when homozygous. However, not all KIT alleles currently identified as "dominant white" have been proven lethal, and in fact W20 is known to be viable in the homozygous form.

The similarities between Dominant White and Sabino 1 reflect their common molecular origin: The W series and SB1 have both been mapped to KIT. The researchers who mapped Sabino 1 in 2005 suggested that other sabino-like patterns might also map to KIT, which has been the case for many other alleles discovered since that time, including major alleles for white leg and facial markings that have also been mapped to or near to the KIT gene.

### Molecular genetics

The KIT gene encodes a protein called steel factor receptor, which is critical to the differentiation of stem cells into blood cells, sperm cells, and pigment cells. A process called alternative splicing, which uses the information encoded in the KIT gene to make slightly different proteins (isoforms) for use in different circumstances, may impact whether a mutation on KIT affects blood cells, sperm cells, or pigment cells. Steel factor receptor interacts chemically with steel factor or stem cell factor to relay chemical messages. These messages are used during embryonic development to signal the migration of early melanocytes (pigment cells) from the neural crest tissue to their eventual destinations in the dermal layer. The neural crest is a transient tissue in the embryo that lies along the dorsal line. Melanocytes migrate along the dorsal line to a number of specific sites: near the eye, near the ear, and the top of the head; six sites along each side of the body, and a few along the tail. At these sites, the cells undergo a few rounds of replication and differentiation, and then migrate down and around the body from the dorsal aspect towards the ventral aspect and the limb buds.

The timing of this migration is critical; all white markings, from a small star to a pure white coat, are caused by the failed migration of melanocytes.

A certain degree of the eventual amount of white, and its "design", is completely random. The development of an organism from single-celled to fully formed is a process with many, many steps. Even beginning with identical genomes, as in clones and identical twins, the process is unlikely to occur the same way twice. A process with this element of randomness is called a stochastic process, and cell differentiation is, in part, a stochastic process. The stochastic element of development is partly responsible for the eventual appearance of white on a horse, potentially accounting for nearly a quarter of the phenotype. The research team that studied dominant white cited "subtle variations in the amount of residual KIT protein" as a potential cause for the variability in phenotype of horses with the same allele. They also speculated that variability in the phenotype of horses with W1 might be caused by "different efficacies of [nonsense-mediated decay] in different individuals and in different body regions." That is, some horses destroy more of the mutant KIT protein than others.

### Lethality

Early embryonal lethality, also known as early embryonic death or a non-viable embryo, may occur when the embryo possesses two copies of certain dominant white alleles. The reason for this is that several mutations of W are caused by nonsense mutations, frameshift mutations or DNA deletions, which, if homozygous, would make it impossible to produce a functional KIT protein. However, it appears that not all W alleles are embryonic lethals. Homozygous embryos from alleles of certain missense and splice site mutations are sometimes viable, apparently because they have less effect on gene function. For instance, W1 is a nonsense mutation and it is thought that horses with the genotype W1/W1 would die in utero, while W20 is a missense mutation and living horses with the W20/W20 genotype have been found. A 2013 study also located horses that were compound W5/W20 heterozygotes, almost completely white, essentially with greater depigmentation than could be accounted for by either allele alone.

## "White" horses that are not dominant white

White horses are potent symbols in many cultures. An array of horse coat colors may be identified as "white", often inaccurately, and many are genetically distinct from "dominant white".

"Albino" horses have never been documented, despite references to so-called "albino" horses. Dominant white is caused by the absence of pigment cells (melanocytes), whereas albino animals have a normal distribution of melanocytes. Also, a diagnosis of albinism in humans is based on visual impairment, which has not been described in horses with dominant white nor similar coat colors. In other mammals, the diagnosis of albinism is based on the impairment of tyrosinase production. No mutations of the tyrosinase gene are known in horses, however, cream and pearl colors result from mutations to a protein involved in tyrosinase transport.

### Non-white colors

- Cremello or Blue-eyed cream horses have rosy pink skin, pale blue eyes and cream-colored coats, indicating that pigment cells and pigment are present in the skin, eyes, and coat, but at lower levels. White horses do not have pigment cells, and thus no pigment, in the skin or coat. In addition, dominant white horses seldom have blue eyes. Other genetic factors, or combinations of genetic factors, such as the pearl gene or champagne gene, can also produce cremello-like coats. These coat colors may be distinguishable from dominant white by their unusually colored eyes.
- Gray horses are born any color and progressively replace their colored coat with gray and white hairs. Most gray horses have dark skin, unless they happen to also carry genes for pink or unpigmented skin. Unlike white horses, grays are not born white, nor is their skin color affected by their coat color change.
- Leopard complex horses, such as the Appaloosa and Knabstrupper breeds, are genetically quite distinct from all other white spotting patterns. The fewspot leopard pattern, however, can resemble white. Two factors influence the eventual appearance of a leopard complex coat: whether one copy or two copies of the Leopard alleles are present, and the degree of dense leopard-associated white patterning that is present at birth. If a foal is homozygous for the LP allele and has extensive dense white patterning, they will appear nearly white at birth, and may continue to lighten with age. In other parts of the world, these horses are called "white born." "White born" foals are less common among Appaloosa horses, which tend to have blankets and varnish roans, than Knabstruppers or Norikers, which tend to be full leopards.

- Tovero, Medicine hat or War bonnet are terms sometimes applied to Pinto horses with residual non-white areas only around the head, especially the ears and poll, while most of the remaining coat is white. While dominant white horses may have areas of residual pigment only around the ears and poll, the term "medicine hat" usually refers to horses with more commonly known white spotting genes, most often tobiano, combined with frame overo, sabino or splashed white.

### Lethal white overo

Foals with lethal white syndrome (LWS) have two copies of the frame overo gene and are born with white or nearly white coats and pink skin. However, unlike dominant white horses, foals with LWS are born with an underdeveloped colon that is untreatable, and if not euthanized, invariably die of colic within a few days of birth. Horses that carry only one allele of the LWS gene are healthy and typically exhibit the "frame overo" spotting pattern. In cases of "solid" horses with frame overo ancestry, uncertain "overo" (non-tobiano) phenotype, or horses with multiple patterns, the LWS allele can be detected by DNA test.

### Mosaicism

Mosaicism in horses is thought to account for some spontaneous occurrences of white, near-white, spotted, and roan horses. Mosaicism refers to mutations that occur after the single-cell stage, and therefore affect only a portion of the adult cells. Mosaicism may be one possible cause for the rare occurrence of brindle coloring in horses. Mosaic-white horses would be visually indistinguishable from dominant whites. Mosaicism could produce white or partially white foals if a stem cell in the developing foal underwent a mutation, or change to the DNA, that resulted in unpigmented skin and hair. The cells that descend from the affected stem cell will exhibit the mutation, while the rest of the cells are unaffected.

A mosaic mutation may or may not be inheritable, depending on the cell populations affected. Though this is not always the case, genetic mutations can occur spontaneously in one sex cell of a parent during gametogenesis. In these cases, called germline mutations, the mutation will be present in the single-celled zygote conceived from the affected sperm or egg cell, and the condition can be inherited by the next generation.

## History of dominant white research

Dominant white horses were first described in scientific literature in 1912. Horse breeder William P. Newell described his family of white and near-white horses to researcher A. P. Sturtevant of Columbia University:

> "The colour of skin is white or so-called pink, usually with a few small dark specks in skin. Some have a great many dark spots in skin. These latter usually have a few dark stripes in hoofs; otherwise the hoofs are almost invariably white. Those that do not have dark specks in skin usually have glass or watch eyes, otherwise dark eyes ... I have one colt coming one year old that is pure white, not a coloured speck on him, not a coloured hair on him, and with glass [blue] eyes."

Sturtevant and his contemporaries agreed that this colt's blue eyes were inherited separately from his white coat. In 1912, Sturtevant assigned the "white" trait to the White or W locus. At the time there was no means of assigning W to a position on the chromosome, or to a gene.

This family of white horses produced Old King in 1908, a dark-eyed white stallion that was purchased by Caleb R. and Hudson B. Thompson. Old King was bred to Morgan mares to produce a breed of horse known today as the American White Horse. A grandson of Old King, Snow King, was at the center of the first major study of the dominant white coat color in horses, conducted in 1969 by Dr. William L. Pulos of Alfred University and Dr. Frederick B. Hutt of Cornell. They concluded, based on test matings and progeny phenotype ratios, that the white coat was dominantly inherited and embryonic lethal in the homozygous state. Other factors, such as variations in expressivity and the influence of multiple genes, may have influenced the progeny ratios that Pulos and Hutt observed. The white coat of the American White Horse has not yet been mapped.

A 1924 study by C. Wriedt identified a heritable white coat color in the Frederiksborg horse. Wriedt described a range of what he considered to be homozygote phenotypes: all-white, white with pigmented flecks, or weißgraue, which transliterates to "white-gray." The German term for gray horse is schimmel, not weißgraue. Heterozygotes, according to Wriedt, ranged from roaned or diluted to more or less solid white horses. Reviewers, such as Miguel Odriozola, reinterpreted Wriedt's data in successive years, while Pulos and Hutt felt that his work had been "erroneous" because Wriedt never concluded that white was lethal when homozygous.

Other researchers prior to modern DNA analysis developed remarkably prescient theories. The gene itself was first proposed and named W in 1948. In a 1969 work on horse coat colors, A los colores del caballo, Miguel Odriozola suggested that various forms of dominantly inherited white spotting might be arranged sequentially along one chromosome, thus allowing for the varied expression of dominant white. He also proposed that other, distant genes might also influence the amount of white present.

The embryonic lethality hypothesis was originally supported by Pulos and Hutt's 1969 study of Mendelian progeny ratios. Conclusions about Mendelian traits that are controlled by a single gene can be drawn from test breedings with large sample sizes. However, traits that are controlled by allelic series or multiple loci are not Mendelian characters, and may not be subject to Mendelian ratios.

Pulos and Hutt knew that if the allele that created a white coat was recessive, then white horses would have to be homozygous for the condition and therefore breeding white horses together would always result in a white foal. However, this did not occur in their study and they concluded that white was not recessive. Conversely, if a white coat was a simple autosomal dominant, ww horses would be non-white, while both Ww and WW horses would be white, and the latter would always produce white offspring. But Pulos and Hutt did not observe any white horses that always produced white offspring, suggesting that homozygous dominant (WW) white horses did not exist. As a result, Pulos and Hutt concluded that white was semidominant and lethal in the homozygous state: ww horses were non-white, Ww were white, and WW died.

Pulos and Hutt reported that neonatal death rates in white foals were similar to those in non-white foals, and concluded that homozygous white fetuses died during gestation. No aborted fetuses were found, suggesting that death occurred early on in embryonic or fetal development and that the fetus was "resorbed."

Prior to Pulos and Hutt's work, researchers were split on the mode of inheritance of white and whether it was deleterious (harmful). Recent research has discovered several possible genetic pathways to a white coat, so disparities in these historical findings may reflect the action of different genes. It is also possible that the varied origins of Pulos and Hutt's white horses might be responsible for the lack of homozygotes. It now appears that not all equine dominant white mutations cause embryonic lethality in the homozygous state.

The white (W) locus was first recognized in mice in 1908. The mutation of the same name produces a belly spot and interspersed white hairs on the dorsal aspect of the coat in the heterozygote (W/+) and black-eyed white in the homozygote (W/W). While heterozygotes are healthy, homozygous W mice have severe macrocytic anemia and die within days. A mutation which affects multiple systems is "pleiotropic." Following the mapping of the KIT gene to the W locus in 1988, researchers began identifying other mutations as part of an allelic series of W. There are dozens of known alleles, each representing a unique mutation on the KIT gene, which primarily produce white spotting from tiny head spots to fully white coats, macrocytic anemia from mild to lethal, and sterility. Some alleles, such as splash produce white spotting alone, while others affect the health of the animal even in the heterozygous state. Alleles encoding small amounts of white are no more likely to be linked with anemia and sterility than those encoding conspicuous white. Presently, no anecdotal or research evidence has suggested that equine KIT mutations affect health or fertility. A recent study showed that blood parameters in horses with the W1 mutation were normal.

Between the time of Pulos and Hutt's study in 1969 and the beginning of molecular-level research into dominant white in the 21st century, a pattern known as "Sabino" began to describe certain white phenotypes. The first allele of the W series identified by researchers was an incomplete dominant that was named Sabino-1 (SB-1). It is found on the same locus as other W alleles. When homozygous, SB-1 can produce nearly all-white horses.

In 2007, researchers from Switzerland and the United States published a paper identifying the genetic cause of dominant white spotting in horses from the Franches Montagnes horse, Camarillo White Horse, Arabian horse and Thoroughbred breeds. Each of these dominant white conditions had occurred separately and spontaneously in the past 75 years, and each represents a different allele (variation or form) of the same gene. These same researchers identified a further seven unique causes of dominant white in 2009: three in distinct families of Thoroughbreds, one Icelandic horse, one Holsteiner, a large family of American Quarter Horses and a family of South German Draft horses.

## Homologous conditions

In humans, a skin condition called piebaldism is caused by more than a dozen distinct mutations in the KIT gene. Piebaldism in humans is characterized by a white forelock, and pigmentless patches of skin on the forehead, brow, face, ventral trunk and extremities. Outside of pigmentation, piebaldism is an otherwise benign condition. In pigs, the "patch," "belted," and commercial "white" colors are caused by mutations on the KIT gene. The best-known model for KIT gene function is the mouse, in which over 90 alleles have been described. The various alleles produce everything from white toes and blazes to black-eyed white mice, panda-white to sashed and belted. Many of these alleles are lethal in the homozygous state, lethal when combined, or sublethal due to anemia. Male mice with KIT mutations are often sterile.

Horse coat color and its genetics