Rapid compensation for glycosylphosphatidylinositol anchor deficient keratinocytes after birth: Visualization of glycosylphosphatidylinositol-anchored proteins in situ

Xing Hua Gao, Gen Kondoh, Masahito Tarutani, Mariko Chikuma, Shintaro Inoue, Tomoko Nakanishi, Masaru Okabe, Yuji Yamaguchi, Kunihiko Yoshikawa, Satoshi Itami, Junji Takeda

Research output: Contribution to journalArticle

2 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)998-1002
Number of pages5
JournalJournal of Investigative Dermatology
Volume118
Issue number6
DOIs
Publication statusPublished - 2002
Externally publishedYes

Fingerprint

Glycosylphosphatidylinositols
Keratinocytes
Visualization
Parturition
Swine
Proteins
Epidermis
Knockout Mice
Genes
Compensation and Redress
X Chromosome Inactivation
X-Linked Genes
Biosynthesis
Chromosomes
Transgenic Mice
Skin
Cells
Phenotype
Tissue
Water

Keywords

  • Cre
  • EGFP
  • loxP
  • Pig-a
  • X-inactivation

ASJC Scopus subject areas

  • Dermatology

Cite this

Rapid compensation for glycosylphosphatidylinositol anchor deficient keratinocytes after birth : Visualization of glycosylphosphatidylinositol-anchored proteins in situ. / Gao, Xing Hua; Kondoh, Gen; Tarutani, Masahito; Chikuma, Mariko; Inoue, Shintaro; Nakanishi, Tomoko; Okabe, Masaru; Yamaguchi, Yuji; Yoshikawa, Kunihiko; Itami, Satoshi; Takeda, Junji.

In: Journal of Investigative Dermatology, Vol. 118, No. 6, 2002, p. 998-1002.

Research output: Contribution to journalArticle

Gao, Xing Hua ; Kondoh, Gen ; Tarutani, Masahito ; Chikuma, Mariko ; Inoue, Shintaro ; Nakanishi, Tomoko ; Okabe, Masaru ; Yamaguchi, Yuji ; Yoshikawa, Kunihiko ; Itami, Satoshi ; Takeda, Junji. / Rapid compensation for glycosylphosphatidylinositol anchor deficient keratinocytes after birth : Visualization of glycosylphosphatidylinositol-anchored proteins in situ. In: Journal of Investigative Dermatology. 2002 ; Vol. 118, No. 6. pp. 998-1002.
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AU - Tarutani, Masahito

AU - Chikuma, Mariko

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AU - Nakanishi, Tomoko

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AU - Takeda, Junji

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