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EMS1 and BRI1 control separate biological processes via extracellular domain diversity and intracellular domain conservation

Author

Listed:
  • Bowen Zheng

    (Shaanxi Normal University)

  • Qunwei Bai

    (Shaanxi Normal University)

  • Lei Wu

    (Shaanxi Normal University)

  • Huan Liu

    (Shaanxi Normal University)

  • Yuping Liu

    (Shaanxi Normal University)

  • Weijun Xu

    (Shaanxi Normal University)

  • Guishuang Li

    (Shaanxi Normal University)

  • Hongyan Ren

    (Shaanxi Normal University)

  • Xiaoping She

    (Shaanxi Normal University)

  • Guang Wu

    (Shaanxi Normal University)

Abstract

In flowering plants, EMS1 (Excess Microsporocytes 1) perceives TPD1 (Tapetum Determinant 1) to specify tapeta, the last somatic cell layer nurturing pollen development. However, the signaling components downstream of EMS1 are relatively unknown. Here, we use a molecular complementation approach to investigate the downstream components in EMS1 signaling. We show that the EMS1 intracellular domain is functionally interchangeable with that of the brassinosteroid receptor BRI1 (Brassinosteroid Insensitive 1). Furthermore, expressing EMS1 together with TPD1 in the BRI1 expression domain could partially rescue bri1 phenotypes, and led to the dephosphorylation of BES1, a hallmark of active BRI1 signaling. Conversely, expressing BRI1 in the EMS1 expression domain could partially rescue ems1 phenotypes. We further show that PpEMS1 and PpTPD1 from the early land plant Physcomitrella patens could completely rescue ems1 and tpd1 phenotypes, respectively. We propose that EMS1 and BRI1 have evolved distinct extracellular domains to control different biological processes but can act via a common intracellular signaling pathway.

Suggested Citation

  • Bowen Zheng & Qunwei Bai & Lei Wu & Huan Liu & Yuping Liu & Weijun Xu & Guishuang Li & Hongyan Ren & Xiaoping She & Guang Wu, 2019. "EMS1 and BRI1 control separate biological processes via extracellular domain diversity and intracellular domain conservation," Nature Communications, Nature, vol. 10(1), pages 1-10, December.
  • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-12112-w
    DOI: 10.1038/s41467-019-12112-w
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