Essential role for Max in early embryonic growth and development.
Loss of Max function in the mouse resulted in generalized developmental arrest of both embryonic and extraembryonic tissues at early postimplantation (approximately E5.5-6.5), coincident with loss or dilution of maternal Max stores in the expanding embryo in vivo and in blastocyst outgrowths in vitro. Developmentally arrested embryos were reduced in size and exhibited widespread cytological degeneration and feeble BrdU incorporation. Max and, by extension, the Myc superfamily, serve essential roles in early mammalian development and a maternal reservoir of Max exists in sufficient amount to sustain Myc superfamily function through preimplantation stages of development.
Shen-Li
H
H
Department of Microbiology and Immunology, Albert Einstein College of Medicine, New York, New York 10461 USA.
O'Hagan
R C
RC
Hou
H
H
Horner
J W
JW
Lee
H W
HW
DePinho
R A
RA
D000818:Animals; D001483:Base Sequence; D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; D050976:Basic-Leucine Zipper Transcription Factors; D017931:DNA Primers; D004268:DNA-Binding Proteins / Q000235:genetics / Q000502:physiology*; D005314:Embryonic and Fetal Development / Q000502:physiology*; D018507:Gene Expression Regulation, Developmental; D020287:In Situ Nick-End Labeling; D051379:Mice; D010641:Phenotype; D014157:Transcription Factors
D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; D050976:Basic-Leucine Zipper Transcription Factors; D017931:DNA Primers; D004268:DNA-Binding Proteins; C067850:Myc associated factor X; D014157:Transcription Factors; C068422:Max protein, mouse