Expression of myc-family, myc-interacting, and myc-target genes during preimplantation mouse development.
Previous studies indicated that members of the myc gene family may be essential for preimplantation development. Other studies revealed that preimplantation embryos lacking c-myc, N-myc, or L-myc are viable, indicating that these genes are either not essential for preimplantation development or can be substituted for functionally by other myc gene family members. To investigate the possible role of these genes during preimplantation development, we determined the temporal patterns of expression of four members of the myc gene family, genes encoding myc-associated proteins, and four putative MYC target genes. We observed a sequential pattern of myc gene expression, with the L-myc mRNA expressed as a maternal transcript, the c-myc mRNA expressed during the 4-cell through morula stages, and the B-myc mRNA expressed highly at the morula and blastocysts stages. B-myc was the predominant family member expressed during preimplantation development. The mxi mRNA was not detectable and the mad mRNA was detectable only as a maternal transcript. The max mRNA, however, was expressed both as a maternal mRNA and as an embryonic message throughout most of preimplantation development. Three putative MYC target genes (Odc, cyclin E, and prothymosin-alpha) were transcriptionally induced during the 2-cell stage, and their mRNAs increased sharply in abundance during development to the morula and blastocyst stages. Another putative MYC target gene, cyclin A, was expressed both as a maternal mRNA and as an embryonic transcript. These data support the view that the expression of myc target genes may be supported initially through the expression of maternally inherited MYC proteins and corresponding mRNAs and that subsequent stage-specific changes in expression of myc genes, myc-associated genes, and myc target genes may control early differentiative events around the time of implantation.
Domashenko
A D
AD
Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.
Latham
K E
KE
Hatton
K S
KS
D000546:Amanitins / Q000494:pharmacology; D000818:Animals; D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; D050976:Basic-Leucine Zipper Transcription Factors; D001755:Blastocyst / Q000378:metabolism*; D002454:Cell Differentiation; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D016213:Cyclins / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics; D005314:Embryonic and Fetal Development; D005260:Female; D018507:Gene Expression Regulation, Developmental; D016259:Genes, myc / Q000235:genetics*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009028:Morula / Q000378:metabolism; D009865:Oocytes / Q000378:metabolism; D009955:Ornithine Decarboxylase / Q000235:genetics; D011498:Protein Precursors / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D012097:Repressor Proteins; D013947:Thymosin / Q000031:analogs & derivatives / Q000235:genetics; D014157:Transcription Factors; D014158:Transcription, Genetic
D000546:Amanitins; D051778:Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; D050976:Basic-Leucine Zipper Transcription Factors; D006063:Chorionic Gonadotropin; D016213:Cyclins; D004268:DNA-Binding Proteins; C499479:Mad protein, mouse; C067850:Myc associated factor X; D011498:Protein Precursors; D012333:RNA, Messenger; D012097:Repressor Proteins; D014157:Transcription Factors; C040782:prothymosin alpha; C068422:Max protein, mouse; D013947:Thymosin; D009955:Ornithine Decarboxylase