The bifunctional abiotic stress signalling regulator and endogenous RNA silencing suppressor FIERY1 is required for lateral root formation
KAUST DepartmentBiological and Environmental Science and Engineering (BESE) Division
Center for Desert Agriculture
Plant Stress Genomics Research Lab
Online Publication Date2010-09-28
Print Publication Date2010-12
Permanent link to this recordhttp://hdl.handle.net/10754/561567
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AbstractThe Arabidopsis FIERY1 (FRY1) locus was originally identified as a negative regulator of stress-responsive gene expression and later shown to be required for suppression of RNA silencing. In this study we discovered that the FRY1 locus also regulates lateral root formation. Compared with the wild type, fry1 mutant seedlings generated significantly fewer lateral roots under normal growth conditions and also exhibited a dramatically reduced sensitivity to auxin in inducing lateral root initiation. Using transgenic plants that overexpress a yeast homolog of FRY1 that possesses only the 3', 5'-bisphosphate nucleotidase activity but not the inositol 1-phosphatase activity, we demonstrated that the lateral root phenotypes in fry1 result from loss of the nucleotidase activity. Furthermore, a T-DNA insertion mutant of another RNA silencing suppressor, XRN4 (but not XRN2 or XRN3), which is an exoribonuclease that is inhibited by the substrate of the FRY1 3', 5'-bisphosphate nucleotidase, exhibits similar lateral root defects. Although fry1 and xrn4 exhibited reduced sensitivity to ethylene, our experiments demonstrated that restoration of ethylene sensitivity in the fry1 mutant is not sufficient to rescue the lateral root phenotypes of fry1. Our results indicate that RNA silencing modulated by FRY1 and XRN4 plays an important role in shaping root architecture. © 2010 Blackwell Publishing Ltd.
CitationCHEN, H., & XIONG, L. (2010). The bifunctional abiotic stress signalling regulator and endogenous RNA silencing suppressor FIERY1 is required for lateral root formation. Plant, Cell & Environment, 33(12), 2180–2190. doi:10.1111/j.1365-3040.2010.02218.x
SponsorsWe thank Dr. John Celenza for the cyc1ATDB:GUS plasmid and Dr. Jian-Kang Zhu for critical reading of the paper. This study was supported by National Science Foundation grant #0446359 and United States Department of Agriculture National Research Initiative competitive grant #2004-02111 (to L. Xiong).
JournalPlant, Cell & Environment
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