• Register
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.


Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.


Inducible mEDA-A1 transgene mediates sebaceous gland hyperplasia and differential formation of two types of mouse hair follicles.

EDA splice isoforms EDA-A1 and EDA-A2 belong to the TNF ligand family and regulate skin appendage formation by activating NF-kappa B- and JNK- promoted transcription. To analyze their action further, we conditionally expressed the isoforms as tetracycline ('Tet')-regulated transgenes in Tabby (EDA-negative) and wild-type mice. Expression of only the mEDA-A1 transgene had two types of effects during embryogenesis: (1) determinative effects on sweat glands and hair follicles. In Tabby mice, one type of hair follicle ('guard hair') was restored, whereas a second type, the dominant undercoat hair follicle ('zigzag') was not; furthermore, the transgene sharply suppressed zigzag hair formation in wild-type mice, with the overall numbers of back hair follicles remaining the same; and (2) trophic effects on sebaceous and Meibomian glands. Marked hyperplasia resulted from expansion of the sebocyte-producing zone in sebaceous glands, with particularly high expression of the transgene and the replication marker PCNA, and correspondingly high production of sebum. The phenotypic effects of mEDA-A1 on sebaceous glands, but not on hair follicles, were reversed when the gene was repressed in adult animals. The results thus reveal both initiating and trophic isoform-specific effects of the EDA gene, and suggest a possible balance of isoform interactions in skin appendage formation.

Pubmed ID: 14506134


  • Cui CY
  • Durmowicz M
  • Ottolenghi C
  • Hashimoto T
  • Griggs B
  • Srivastava AK
  • Schlessinger D


Human molecular genetics

Publication Data

November 15, 2003

Associated Grants


Mesh Terms

  • Animals
  • Cell Differentiation
  • Cell Division
  • Ectodysplasins
  • Enzyme Activation
  • Gene Expression Regulation
  • Hair Follicle
  • Hyperplasia
  • JNK Mitogen-Activated Protein Kinases
  • Membrane Proteins
  • Mice
  • Mice, Mutant Strains
  • Mice, Transgenic
  • Mitogen-Activated Protein Kinases
  • Models, Biological
  • NF-kappa B
  • Proliferating Cell Nuclear Antigen
  • Protein Isoforms
  • Protein Synthesis Inhibitors
  • RNA, Messenger
  • Sebaceous Glands
  • Sebum
  • Tetracycline
  • Transcription, Genetic
  • Transgenes