Abstract
BackgroundDuring pregnancy, the mammary glands from Id2 mutant animals are deficient in lobulo-alveolar development. This failure of development is believed to be due to a proliferation defect.MethodsWe have asked whether functional Id2 expression is necessary for Wnt induced mammary hyperplasia, side branching, and cancer, by generating mice expressing a Wnt1 transgene in an Id2 mutant background.ResultsWe show in this work that forced expression of Wnt1 in the mammary gland is capable of overcoming the block to proliferation caused by the absence of Id2. We also show that Wnt1 expression is able to cause mammary tumors in an Id2 mutant background.ConclusionsWe conclude that functional Id2 expression is not required for Wnt1 to induce mammary hyperplasia and mammary tumors.
Highlights
During pregnancy, the mammary glands from Id2 mutant animals are deficient in lobulo-alveolar development
Id proteins act as dominant inhibitors of Basic helix-loop-helix (bHLH) transcription factors by blocking their ability to bind to DNA and activate gene transcription [2,3]
We used mice carrying a transgene in which Wnt1 is under the control of the promoter of the Mouse Mammary Tumor Virus (MMTV-Wnt1 Tg) [7] and we crossed these to Id2 loss of function mutant mice [4,8]
Summary
The mammary glands from Id2 mutant animals are deficient in lobulo-alveolar development. This failure of development is believed to be due to a proliferation defect. Basic helix-loop-helix (bHLH) transcription factors such as MyoD, E12, and E47 are key regulators of gene expression and control many differentiation events during development [1,2,3]. These transcription factors bind E-box or E-box-like sequences as homo-or heterodimers, and control the transcription of target genes containing these sequences in their promoters. Since the bHLH proteins regulate cell-type specific gene expression during cell commitment and differentiation, the formation of inactive heterodimers of bHLH proteins with Id proteins inhibits the commitment and differentiation the bHLH proteins promote
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