When recognized by the spliceosome, the sequence between the original and duplicated AGGT will be spliced, resulting in the creation of an intron without alteration of the coding sequence of the gene. Double-stranded break repair via non-homologous end joining was recently identified as a source of intron gain when researchers identified short direct repeats flanking 43% of gained introns in Daphnia. These numbers must be compared to the number of conserved introns flanked by repeats in other organisms, though, for statistical relevance. For group II intron insertion, the retrohoming of a group II intron into a nuclear gene was proposed to cause recent spliceosomal intron gain. Intron transfer has been hypothesized to result in intron gain when a paralog or pseudogene gains an intron and then transfers this intron via recombination to an intron-absent location in its sister paralog. Intronization is the process by which mutations create novel introns from formerly exonic sequence. Thus, unlike other proposed mechanisms of intron gain, this mechanism does not require the insertion or generation of DNA to create a novel intron.The only hypothesized mechanism of recent intron gain lacking any direct evidence is that of group II intron insertion, which when demonstrated in vivo, abolishes gene expression. Group II introns are therefore likely the presumed ancestors of spliceosomal introns, acting as site-specific retroelements, and are no longer responsible for intron gain.
Through examinations in families it was found that there is a family connection to the occurrences, which leads to the conclusion that there is a genetic predisposition for it; for example, patients with folliculitis decalvans could have a hereditary different opening of the hair follicle that could facilitate the lodging of the bacteria. Immunologically, another possibility is that especially strong intercellular fixation protein ICAM-1 contributes to inflammation with its strong effect of attracting white blood cells such as granulocytes and lymphocytes. Diagnosis
Management
Some sufferers have found that a daily intake of MSM helps relieve the inflammation and scarring that comes with chronic Folliculitis decalvans. Epidemiology
This disorder was first described by Charles-Eugène Quinquaud in 1888. He isolated bacteria from the hair follicles of affected patients and introduced them in rats, mice and rabbits, with no result. In 1905 it was then differentiated from other scarring alopecias and the name Folliculitis decalvans, that remains current, was introduced. About 11% of the occurrences of scarring alopecias are of this type. Men are more commonly affected than women and its appearance is usually between the late teens and middle adult years. According to studies in the United States, African Americans are more frequently affected than White Americans. See also
Cicatricial alopecia

References


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