Sundberg J P, Boggess D, Hogan M E, Sundberg B A, Rourk M H, Harris B, Johnson K, Dunstan R W, Davisson M T
Jackson Laboratory, Bar Harbor, Maine 04609-1500, USA.
Am J Pathol. 1997 Jul;151(1):293-310.
The harlequin ichthyosis (ichq) mouse mutation arose spontaneously in 1989 in a colony of BALB/cJ mice at The Jackson Laboratory. Affected mice developed thick skin due to formation of compact, orthokeratotic scales that fractured over articular surfaces, secondary to bending. Harlequin ichthyosis mice on the inbred BALB/cJ background died between 9 and 12 days of age. Onset of the clinical phenotype corresponded with emergence of hair fibers from follicles at 5 days of age. There was marked proliferation of the root sheaths of anagen hair follicles, limited to the region within the dermis. Sebaceous glands were present but small compared with those of littermate controls. Emerging hair fibers were surrounded by a thick, compact sheath of cornified cells. Mutant skin contained large mitochondria with lamellar-shaped, electron-dense structures at the ultrastructural level. Keratohyalin granules were smaller and less pleomorphic than those in control mice. Lamellar bodies were not evident in either mutant or littermate control mice. Using a panel of antibodies to evaluate changes in keratinocyte differentiation, mouse-specific keratin 6 was overexpressed in the suprabasilar, hyperplastic epidermis. Loricrin expression, within the cytoplasm of cells in the stratum granulosum, decreased rapidly postmortem, unlike that in normal mice where it was stable for over 24 hours postmortem. Filaggrin expression, within granules of cells in the stratum granulosum, was prominent, corresponding to hypergranulosis evident by light microscopy in mutant mouse skin. Skin grafts from harlequin ichthyosis mice grafted onto immunodeficient nude mice maintained the phenotype for the 10-week observation period. The mutant gene locus mapped to the proximal end of mouse chromosome 19 and is inherited as a fully penetrant autosomal recessive gene. The harlequin ichthyosis mouse mutation is very similar to human type 2 harlequin ichthyosis for which it may be a good model.
丑角鱼鳞病(ichq)小鼠突变于1989年在杰克逊实验室的一群BALB/cJ小鼠中自发产生。受影响的小鼠由于形成紧密的正角化鳞片而皮肤增厚,这些鳞片在关节表面因弯曲而破裂。近交BALB/cJ背景的丑角鱼鳞病小鼠在9至12日龄时死亡。临床表型的出现与5日龄时毛囊中毛发纤维的出现相对应。生长期毛囊的根鞘有明显增殖,仅限于真皮内区域。皮脂腺存在,但与同窝对照相比较小。新生的毛发纤维被一层厚厚的、紧密的角质化细胞鞘包围。在超微结构水平上,突变皮肤含有大的线粒体,带有层状的、电子致密结构。透明角质颗粒比对照小鼠的更小且多形性更低。板层小体在突变小鼠或同窝对照小鼠中均不明显。使用一组抗体评估角质形成细胞分化的变化,小鼠特异性角蛋白6在基底上层增生的表皮中过度表达。与正常小鼠死后24小时以上稳定表达不同,颗粒层细胞胞质内的兜甲蛋白表达在死后迅速下降。颗粒层细胞颗粒内的丝聚合蛋白表达突出,这与突变小鼠皮肤光镜下明显的颗粒层增厚相对应。将丑角鱼鳞病小鼠的皮肤移植到免疫缺陷的裸鼠上,在10周的观察期内维持了该表型。突变基因座定位于小鼠19号染色体近端,作为一个完全显性的常染色体隐性基因遗传。丑角鱼鳞病小鼠突变与人类2型丑角鱼鳞病非常相似,它可能是研究人类2型丑角鱼鳞病的良好模型。