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Lamin B1 is required for mature neuron-specific gene expression during olfactory sensory neuron differentiation

Author

Listed:
  • Crystal M. Gigante

    (The Johns Hopkins University
    Carnegie Institution for Science)

  • Michele Dibattista

    (Monell Chemical Senses Center
    Neuroscience and Sensory Organs, University of Bari ‘A. Moro’)

  • Frederick N. Dong

    (The Johns Hopkins University)

  • Xiaobin Zheng

    (Carnegie Institution for Science)

  • Sibiao Yue

    (Carnegie Institution for Science)

  • Stephen G. Young

    (University of California)

  • Johannes Reisert

    (Monell Chemical Senses Center)

  • Yixian Zheng

    (Carnegie Institution for Science)

  • Haiqing Zhao

    (The Johns Hopkins University)

Abstract

B-type lamins are major constituents of the nuclear lamina in all metazoan cells, yet have specific roles in the development of certain cell types. Although they are speculated to regulate gene expression in developmental contexts, a direct link between B-type lamins and developmental gene expression in an in vivo system is currently lacking. Here, we identify lamin B1 as a key regulator of gene expression required for the formation of functional olfactory sensory neurons. By using targeted knockout in olfactory epithelial stem cells in adult mice, we show that lamin B1 deficient neurons exhibit attenuated response to odour stimulation. This deficit can be explained by decreased expression of genes involved in mature neuron function, along with increased expression of genes atypical of the olfactory lineage. These results support that the broadly expressed lamin B1 regulates expression of a subset of genes involved in the differentiation of a specific cell type.

Suggested Citation

  • Crystal M. Gigante & Michele Dibattista & Frederick N. Dong & Xiaobin Zheng & Sibiao Yue & Stephen G. Young & Johannes Reisert & Yixian Zheng & Haiqing Zhao, 2017. "Lamin B1 is required for mature neuron-specific gene expression during olfactory sensory neuron differentiation," Nature Communications, Nature, vol. 8(1), pages 1-13, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15098
    DOI: 10.1038/ncomms15098
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