Genetic suppression reveals DNA repair-independent antagonism between BRCA1 and COBRA1 in mammary gland development View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-03-04

AUTHORS

Sreejith J. Nair, Xiaowen Zhang, Huai-Chin Chiang, Jamiul Jahid, Yao Wang, Paula Garza, Craig April, Neeraj Salathia, Tapahsama Banerjee, Fahad S. Alenazi, Jianhua Ruan, Jian-Bing Fan, Jeffrey D. Parvin, Victor X. Jin, Yanfen Hu, Rong Li

ABSTRACT

The breast cancer susceptibility gene BRCA1 is well known for its function in double-strand break (DSB) DNA repair. While BRCA1 is also implicated in transcriptional regulation, the physiological significance remains unclear. COBRA1 (also known as NELF-B) is a BRCA1-binding protein that regulates RNA polymerase II (RNAPII) pausing and transcription elongation. Here we interrogate functional interaction between BRCA1 and COBRA1 during mouse mammary gland development. Tissue-specific deletion of Cobra1 reduces mammary epithelial compartments and blocks ductal morphogenesis, alveologenesis and lactogenesis, demonstrating a pivotal role of COBRA1 in adult tissue development. Remarkably, these developmental deficiencies due to Cobra1 knockout are largely rescued by additional loss of full-length Brca1. Furthermore, Brca1/Cobra1 double knockout restores developmental transcription at puberty, alters luminal epithelial homoeostasis, yet remains deficient in homologous recombination-based DSB repair. Thus our genetic suppression analysis uncovers a previously unappreciated, DNA repair-independent function of BRCA1 in antagonizing COBRA1-dependent transcription programme during mammary gland development. More... »

PAGES

10913

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms10913

DOI

http://dx.doi.org/10.1038/ncomms10913

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1051722373

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26941120


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