4.6 Article

CONSTANS-like 9 (COL9) delays the flowering time in Oryza sativa by repressing the Ehd1 pathway

Journal

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.09.013

Keywords

CONSTANS-Like 9; Flowering; Ehd1; OsRACK1

Funding

  1. 863 High Technology Research and Development Program of China (863 Program) [2011AA10A101]
  2. Specialized Research Fund for the Doctoral Program of Higher Education [20124404120007]

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Flowering or heading is one of most important agronomic traits in rice. It has been characterized that CONSTANS (CO) and CONSTANS-like (COL) proteins are critical flowering regulators in response to photoperiodic stress in plants. We have previously identified that the COL family member OsCOL9 can positively enhance the rice blast resistance. In the present study, we aimed to explore the functional role of OsCOL9 in modulating the photoperiodic flowering. Our data showed that overexpression of OsCOL9 delayed the flowering time under both short-day (SD) and long-day (LD) conditions, leading to suppressed expressions of EHd1, RFT and Hd3a at the mRNA Level. OsCOL9 expression exhibited two types of circadian patterns under different daylight conditions, and it could delay the heading date by suppressing the Ehd1 photoperiodic flowering pathway. In contrast, the expressions of previously reported flowering regulators were not significantly changed in OsCOL9 transgenic plants, indicating that OsCOL9 functioned independently of other flowering pathways. In addition, OsCOL9 served as a potential yield gene, and its deficiency reduced the grain number of main panicle in plants. Furthermore, yeast two-hybrid assay indicated that OsCOL9 physically interacted with Receptor for Activated C-kinase 1 (OsRACK1). Rhythmic pattern analysis suggested that OsRACK1 responded to the change of daylight, which was regulated by the circadian clock. Taken together, our results revealed that OsCOL9 could delay the flowering time in rice by repressing the Ehd1 pathway. (C) 2016 The Authors. Published by Elsevier Inc.

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