In the last half-century, however, a focus on behavioral and genetic testing of mammals has accumulated extensive evidence of at least dichromatic color vision in a number of mammalian orders. Mammals are now usually assumed to be dichromats (possessing S- and L-cones), with monochromats viewed as the exceptions. Two mammalian orders containing marine mammals exhibit monochromatic vision:

Pinnipeds (including seals, sea lions and walruses)
Cetaceans (including dolphins and whales)Unlike the trichromacy exhibited in most primates, Owl monkeys (genus Aotus) are also monochromats. Several members of the family Procyonidae (raccoon, crab-eating raccoon and kinkajou) and a few rodents have been demonstrated as cone monochromats, having lost functionality of the S-cone (retaining the L-cone).The light available in an animals habitat is a significant determiner of a mammals color vision. Marine, Nocturnal or Burrowing mammals, which experience less light, have less evolutionary pressure to preserve dichromacy, so often evolve monochromacy.A recent study using through PCR analysis of genes OPN1SW, OPN1LW, and PDE6C determined that all mammals in the cohort Xenarthra (representing sloths, anteaters and armadillos) developed rod monochromacy through a stem ancestor. See also
Achromatopsia
Blue cone monochromacy
Cone dystrophy
Dichromacy
Trichromacy
Tetrachromacy

References
External links
Rossi, Ethan (February 2013). "Visual Function and Cortical Organization in Carriers of Blue Cone Monochromacy". PLOS ONE. 8 (2): e57956. Bibcode:2013PLoSO...857956R. doi:10.1371/journal.pone.0057956. PMC 3585243. PMID 23469117. Weleber, Richard (June 2002). "Infantile and childhood retinal blindness: A molecular perspective (TheFranceschetti Lecture)". Ophthalmic Genetics. 23 (2): 71–98. doi:10.1076/opge.23.2.71.2214. PMID 12187427. S2CID 30741530.
Low-set ears are the most common cranial dysmorphism seen in 3C syndrome, and ocular coloboma is the least common of the non-concurrent symptoms (cleft lip co-occurring with cleft palate is the least common).Cranial dysplasias associated with 3C syndrome are also reflected in the brain. Besides the cerebellar hypoplasia, cysts are commonly found in the posterior cranial fossa, the ventricles and the cisterna magna are dilated/enlarged, and Dandy–Walker malformation is present. These are reflected in the developmental delays typical of the disease. 75% of children with 3C syndrome have Dandy-Walker malformation and hydrocephalus.Signs and symptoms in other body systems are also associated with 3C syndrome. In the skeletal system, ribs may be absent, and hemivertebrae, syndactyly (fusion of fingers together), and clinodactyly (curvature of the fifth finger) may be present. In the GI and genitourinary systems, anal atresia, hypospadia (misplaced urethra), and hydronephrosis may exist. Adrenal hypoplasia and growth hormone deficiency are associated endocrine consequences of Ritscher-Schinzel syndrome. Some immunodeficiency has also been reported in connection with 3C syndrome. Many children with the disorder die as infants due to severe congenital heart disease. The proband of Ritscher and Schinzels original study was still alive at the age of 21. A fetus with 3C syndrome may have an umbilical cord with one umbilical artery instead of two. Genetics
3C syndrome is an autosomal recessive disease, caused by a mutation on the long arm of chromosome 8 at 8q24.13, the locus for KIAA0196, the gene for the protein strumpellin.