A specific, nonproliferative role for E2F-5 in choroid plexus function revealed by gene targeting.
Homozygous E2F-5 knockout embryos and mice have been generated. Although embryonic development appeared normal, newborn mice developed nonobstructive hydrocephalus, suggesting excessive cerebrospinal fluid (CSF) production. Although the CSF-producing choroid plexus displayed normal cellular organization, it contained abundant electron-lucent epithelial cells, consistent with excessive CSF secretory activity. Moreover, E2F-5 CNS expression in normal animals was largely confined to the choroid plexus. Cell cycle kinetics were not perturbed in homozygous knockout embryo fibroblasts. Thus, E2F-5 is not essential for cell proliferation. Rather, it affects the secretory behavior of a differentiated neural tissue.
Lindeman
G J
GJ
The Dana-Farber Cancer Institute/Harvard Medical School, Boston, Massachusetts 02115, USA.
Dagnino
L
L
Gaubatz
S
S
Xu
Y
Y
Bronson
R T
RT
Warren
H B
HB
Livingston
D M
DM
D000483:Alleles; D000818:Animals; D002455:Cell Division; D002831:Choroid Plexus / Q000378:metabolism / Q000502:physiology*; D050700:E2F5 Transcription Factor; D017353:Gene Deletion; D018390:Gene Targeting; D006801:Humans; D006849:Hydrocephalus / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D014157:Transcription Factors / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*
D050700:E2F5 Transcription Factor; C092558:E2F5 protein, human; C490490:E2f5 protein, mouse; D014157:Transcription Factors