**4. Hyperplasia of the epidermis and sebaceous gland**

In aPKCλ cKO mice, the IFE and sebaceous glands were affected [22, 23]. The thickness of the IFE of the dorsal skin increased in the mutant mice, as revealed by significant expansion of the expression domain for loricrin (a marker for terminal differentiation) and keratin 10 (K10, a marker for spinous cells). Moreover, the sebaceous glands were enlarged in the cKO mice. Accordingly, immunostaining for adipose differentiation-related protein (ADFP, a marker for the surface of lipid droplets) and stearoyl-CoA desaturase 1 (SCD1, a marker for mature sebocytes), and Nile red staining showed remarkable increases in the sebaceous glands of the mutant mice.

Importantly, the expression domain of Lrig1 was expanded in the mutant mice [22, 23]. Lrig1 marks the junctional zone between the infundibulum and the sebaceous gland, and Lrig1 expressing cells contribute to the IFE and sebaceous glands [30]. Thus, this bipotent activity of Lrig1 is thought to be implicated in hyperplasia of these tissues.
