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- Title
Rapid Compensation for Glycosylphosphatidylinositol Anchor Deficient Keratinocytes after Birth: Visualization of Glycosylphosphatidylinositol-Anchored Proteins in situ.
- Authors
Gao, Xing-Hua; Kondoh, Gen; Tarutani, Masahito; Hara, Mariko; Inoue, Shintaro; Nakanishi, Tomoko; Okabe, Masaru; Yamaguchi, Yuji; Yoshikawa, Kunihiko; Itami, Satoshi; Takeda, Junji
- Abstract
Pig-a , an X-linked gene, is a key component of glycosylphosphatidylinositol (GPI) anchor biosynthesis based on the fact that lack of this gene causes deficiencies of hundreds of GPI-anchored proteins. We previously demonstrated an essential role for the GPI-anchor in keratinocyte differentiation using male Pig-a knockout mice (K5-Cre:Pig-a flox ). Here we analyzed keratinocytes of the female K5-Cre: Pig-a flox/+ mice with heterozygous knockout of Pig-a . These cells exhibited the mosaic pattern of GPI-anchor positive and negative expression typical of random inactivation of the X chromosome. The female K5-Cre:Pig-a flox/ + mice appeared slightly wrinkled with dry skin at birth and white scales starting from 4 d after birth without any histologic abnormality. This phenotype was temporary and milder than that seen in the male knockout mice. To characterize the fate of GPI-anchor-positive cells more clearly, we introduced a transgenic mouse line that expresses enhanced green fluorescent protein in GPI-anchored form into female K5-Cre:Pig-a flox/+ mice and monitored GPI-anchor-positive keratinocytes in situ . Within 36 h after birth, the upper layer of the GPI-anchor-negative zone in epidermis was replaced by the GPI-anchor-positive counterpart. This tissue replacement was accompanied by recovery in trans-epidermal water loss over a similar time course. These observations suggest that the GPI-anchoring is associated with the barrier function as well as with organized differentiation of the epidermis after birth.
- Subjects
KERATINOCYTES; SKIN diseases; PHOSPHOINOSITIDES
- Publication
Journal of Investigative Dermatology, 2002, Vol 118, Issue 6, p998
- ISSN
0022-202X
- Publication type
Article
- DOI
10.1046/j.1523-1747.2002.01778.x