• Register
X
Forgot Password

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

X

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.

No
Yes

Early embryonic death of mice deficient in gamma-adaptin.

Intracellular protein transport and sorting by vesicles in the secretory and endocytic pathways requires the formation of a protein coat on the membrane. The heterotetrameric adaptor protein complex 1 (AP-1) promotes the formation of clathrin-coated vesicles at the trans-Golgi network. AP-1 interacts with various sorting signals in the cytoplasmic tails of cargo molecules, thus indicating a function in protein sorting. We generated mutants of the gamma-adaptin subunit of AP-1 in mice to investigate its role in post-Golgi vesicle transport and sorting processes. gamma-Adaptin-deficient embryos develop until day 3.5 post coitus and die during the prenidation period, revealing that AP-1 is essential for viability. In heterozygous mice the amount of AP-1 complexes is reduced to half of controls. Free beta1- or micro1 chains were not detectable, indicating that they are unstable unless they are part of AP-1 complexes. Heterozygous mice weigh less then their wild-type littermates and show impaired T cell development.

Pubmed ID: 10026148

Authors

  • Zizioli D
  • Meyer C
  • Guhde G
  • Saftig P
  • von Figura K
  • Schu P

Journal

The Journal of biological chemistry

Publication Data

February 26, 1999

Associated Grants

None

Mesh Terms

  • Adaptor Protein Complex gamma Subunits
  • Animals
  • Fetal Death
  • Genes, Lethal
  • Heterozygote
  • Membrane Proteins
  • Mice
  • Mutagenesis, Site-Directed
  • Phenotype