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miR-212 and miR-132 are dispensable for mouse mammary gland development

Nature Genetics volume 46, pages 804–805 (2014)Cite this article

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Ucar et al. reply:

MicroRNAs are important regulators of gene expression that are involved in almost all cellular processes. Previously, we showed that the genetic deletion of the miR-212/132 family leads to impaired ductal outgrowth during pubertal mammary gland development in female mice1. Transplantation experiments demonstrated a stromal origin for the phenotype, identified as a lack of terminal end buds (TEBs) and impaired collagen deposition around mammary ducts. We showed that miR-212 and miR-132 are expressed exclusively by mammary stromal cells and target MMP-9. Absence of miR-212 and miR-132 leads to higher MMP-9 levels, resulting in impaired collagen deposition and hyperactivation of transforming growth factor (TGF)-β signaling, which consequently impairs epithelial cell proliferation1,2.

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Figure 1: Differentially deleted genomic regions in the Mir212-Mir132 locus and its evolutionary conservation.

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GenBank/EMBL/DDBJ

Gene Expression Omnibus

References

  1. Ucar, A. et al. Nat. Genet. 42, 1101–1108 (2010).

    Article  CAS  Google Scholar 

  2. Ucar, A., Vafaizadeh, V., Chowdhury, K. & Groner, B. Cell Cycle 10, 563–565 (2011).

    Article  CAS  Google Scholar 

  3. Remenyi, J. et al. PLoS ONE 8, e62509 (2013).

    Article  CAS  Google Scholar 

  4. Kayo, H. et al. Nat. Genet. 46, 802–804 (2013).

    Article  Google Scholar 

  5. Sternlicht, M.D. et al. Development 132, 3923–3933 (2005).

    Article  CAS  Google Scholar 

  6. Chen, W. et al. Cancer Cell 6, 387–398 (2004).

    Article  CAS  Google Scholar 

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Acknowledgements

We are grateful to A. Simon (University of Dundee) for sharing with us full-length targeting construct sequence and G. Eichele for support.

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Author notes

  1. Ahmet Ucar

    Present address: Present address: Wellcome Trust Centre for Cell Matrix Research, Faculty of Life Sciences, University of Manchester, Manchester, UK.,

Authors and Affiliations

  1. Department of Molecular Cell Biology, Max Planck Institute of Biophysical Chemistry, Goettingen, Germany

    Ahmet Ucar, Erdem Erikci & Kamal Chowdhury

  2. Division of Developmental Immunobiology, German Cancer Research Center (DKFZ), Heidelberg, Germany

    Olga Ucar

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  1. Ahmet Ucar
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  2. Erdem Erikci
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  3. Olga Ucar
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  4. Kamal Chowdhury
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Correspondence to Ahmet Ucar or Kamal Chowdhury.

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The authors declare no competing financial interests.

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Ucar, A., Erikci, E., Ucar, O. et al. miR-212 and miR-132 are dispensable for mouse mammary gland development. Nat Genet 46, 804–805 (2014). https://doi.org/10.1038/ng.3032

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