PMID- 10079236
OWN - NLM
STAT- MEDLINE
DCOM- 19990601
LR  - 20220408
IS  - 0950-1991 (Print)
IS  - 0950-1991 (Linking)
VI  - 126
IP  - 8
DP  - 1999 Apr
TI  - Early embryonic lethality in Bmp5;Bmp7 double mutant mice suggests functional
      redundancy within the 60A subgroup.
PG  - 1753-68
AB  - Members of the BMP family of signaling molecules display a high conservation of
      structure and function, and multiple BMPs are often coexpressed in a variety of
      tissues during development. Moreover, distinct BMP ligands are capable of
      activating common pathways. Here we describe the coexpression of two members of
      the 60A subfamily of BMPs, Bmp5 and Bmp7, at a number of different sites in the
      embryo from gastrulation onwards. Previous studies demonstrate that loss of
      either Bmp5 or Bmp7 has negligible effects on development, suggesting these
      molecules functionally compensate for each other at early stages of embryonic
      development. Here we show this is indeed the case. Thus we find that Bmp5;Bmp7
      double mutants die at 10.5 dpc and display striking defects primarily affecting
      the tissues where these factors are coexpressed. The present analysis also
      uncovers novel roles for BMP signaling during the development of the allantois,
      heart, branchial arches, somites and forebrain. Bmp5 and Bmp7 do not appear to be
      involved in establishing pattern in these tissues, but are instead necessary for 
      the proliferation and maintenance of specific cell populations. These findings
      are discussed with respect to potential mechanisms underlying cooperative
      signaling by multiple members of the TGF-beta superfamily.
FAU - Solloway, M J
AU  - Solloway MJ
AD  - Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA
      02138, USA. ejrobert@husc.harvard.edu
FAU - Robertson, E J
AU  - Robertson EJ
LA  - eng
GR  - GM07620/GM/NIGMS NIH HHS/United States
GR  - HD25208/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Development
JT  - Development (Cambridge, England)
JID - 8701744
RN  - 0 (BMP5 protein, human)
RN  - 0 (BMP7 protein, human)
RN  - 0 (Bmp5 protein, mouse)
RN  - 0 (Bone Morphogenetic Protein 5)
RN  - 0 (Bone Morphogenetic Protein 7)
RN  - 0 (Bone Morphogenetic Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
RN  - 344S277G0Z (Allantoin)
SB  - IM
MH  - Allantoin
MH  - Animals
MH  - Apoptosis
MH  - Bone Morphogenetic Protein 5
MH  - Bone Morphogenetic Protein 7
MH  - Bone Morphogenetic Proteins/genetics/*physiology
MH  - Chorion
MH  - Embryonic and Fetal Development
MH  - Epithelium/embryology
MH  - Gastrula
MH  - Gene Expression Regulation, Developmental
MH  - Heart/embryology
MH  - Humans
MH  - Mice
MH  - Morphogenesis
MH  - Mutagenesis
MH  - Neural Crest
MH  - RNA, Messenger
MH  - Somites
MH  - *Transforming Growth Factor beta
EDAT- 1999/03/18 00:00
MHDA- 1999/03/18 00:01
CRDT- 1999/03/18 00:00
PHST- 1999/03/18 00:00 [pubmed]
PHST- 1999/03/18 00:01 [medline]
PHST- 1999/03/18 00:00 [entrez]
AID - 10.1242/dev.126.8.1753 [doi]
PST - ppublish
SO  - Development. 1999 Apr;126(8):1753-68. doi: 10.1242/dev.126.8.1753.