Smad1 and Smad8 function similarly in mammalian central nervous system development.

Abstract:

:Smads 1, 5, and 8 are the intracellular mediators for the bone morphogenetic proteins (BMPs), which play crucial roles during mammalian development. Previous research has shown that Smad1 is important in the formation of the allantois, while Smad5 has been shown to be critical in the process of angiogenesis. To further analyze the BMP-responsive Smads, we disrupted the murine Smad8 gene utilizing the Cre/loxP system. A Smad8 hypomorphic allele (Smad8(Deltaexon3)) was constructed that contains an in-frame deletion of exon 3, removing one-third of the MH2 domain and a small portion of the linker region. Xenopus injection assays indicated that this Smad8 deletion allele is still functional but has reduced ventralizing capability compared to the wild type. Although Smad8(Deltaexon3/Deltaexon3) embryos are phenotypically normal, homozygotes of another hypomorphic allele of Smad8 (Smad8(3loxP)) containing a neomycin cassette within intron 3, phenocopy an embryonic brain defect observed in roughly 22% of Smad1(+/)(-) embryos analyzed at embryonic day 11.5. These observations suggest that BMP-responsive Smads have critical functions in the development of the mammalian central nervous system.

journal_name

Mol Cell Biol

authors

Hester M,Thompson JC,Mills J,Liu Y,El-Hodiri HM,Weinstein M

doi

10.1128/MCB.25.11.4683-4692.2005

subject

Has Abstract

pub_date

2005-06-01 00:00:00

pages

4683-92

issue

11

eissn

0270-7306

issn

1098-5549

pii

25/11/4683

journal_volume

25

pub_type

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