Table 1.
Clinical summary of 169 KOMP strains screened for skin, hair, and nail abnormalities.
Fig 1.
Incidental lesions were found scattered throughout the skin samples in many lines.
Incidental lesions were not consistently found in all mice of a line. Lesions included solitary tail skin hair follicle with infundibular plugging (A-C). Truncal hair follicle infundibular plugging, rupture below the level of the sebaceous gland, follicle filled with neutrophils and surrounded by neutrophils and macrophages (D-F). Sporadic skin lesions found in many mice examined included isolated, one or two, ruptured hair follicles in the dermis where the free hair shaft fragments were engulfed by granulomas and surrounded by neutrophils (G-I). Hematoxylin and eosin stain, bar size indicated in each figure.
Fig 2.
A B6N(Cg)-Far2tm2b(KOMP)Wtsi/2J mutant (left) and wildtype (right) mouse.
Both are 15 week old females. Note the alopecia extending distally from the base of the ears.
Fig 3.
Sebaceous gland changes in fatty acyl CoA reductase 2 mutant mice.
Most late stage anagen hair follicles in B6N(Cg)-Far2tm2b(KOMP)Wtsi/2J mutant mice, as in this 184 day old male, were relatively normal and produced a normal hair shaft (A). However, the sebaceous glands were mildly hypoplastic with brightly eosinophilic mature sebocytes that did not immediately rupture as they entered the infundibulum (C). As in other mouse mutations that cause hypoplasia of sebaceous glands, the hair shafts in these mice did not exit the follicular ostium resulting in perforation of the root sheaths, release of the hair shaft into the dermis, and an inflammatory reaction (B). This healed by follicular scarring, or cicatricial alopecia. By contrast, aged and sex matched B6N(Cg) controls rarely exhibited ruptured follicles (D). Sebaceous glands varied in size with the hair cycle, which was normal, and sebocytes had light pink cytoplasm that becomes very pale as the cells matured and abruptly ruptured into the duct. (E). Hematoxylin and eosin stain, bar size indicated in each figure.
Fig 4.
Follicular dystrophy in fatty acyl CoA reductase 2 mutant mice.
In areas of alopecia, the B6N(Cg)- Far2tm2b(KOMP)Wtsi/2J mutant skin was mildly acanthotic and orthokeratotic, most likely secondary to the abnormal secretions of the sebaceous glands. The infundibulum was mildly dilated (A, B). Follicles with follicular dystrophy (C, D) and with pigment cast (E) were identified occasionally to frequently. Such ruptured follicles with granulomatous inflammation eventually lead to follicular scarring, a form of cicatricial alopecia. Hematoxylin and eosin stain, bar size indicated in each figure.
Fig 5.
Vibrissae dystrophy in some protein phosphatase 1, regulatory subunit 9B mice.
B6N(Cg)-Ppp1r9btm1.1(KOMP)Vlcg/J, had follicular dystrophy limited to many but not all mystacial vibrissae in heterozygous but not homozygous mutant mice suggesting this is an incidental, albeit relatively frequent lesion. Boxed areas are enlarged as indicated by the arrows. Pigment casts are identified in all dystrophic hair follicles (B, F, and H). Hematoxylin and eosin stain, bar size indicated in each figure.