Preparing your results

Forgot Password

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

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