4.8 Article

ABA represses TOR and root meristem activity through nuclear exit of the SnRK1 kinase

出版社

NATL ACAD SCIENCES
DOI: 10.1073/pnas.2204862119

关键词

root; growth control; abscisic acid; energy signaling; target of rapamycin

资金

  1. Fundacao para a Ciencia e a Tecnologia [UIDB/04551/2020, LISBOA-01-0145-FEDER-028128, PTDC/BIA-BID/32347/2017]
  2. EU [867426]
  3. [PPBI-POCI-01-0145-FEDER-022122]

向作者/读者索取更多资源

This study reveals that the plant hormone abscisic acid (ABA) can regulate cell proliferation and root growth by modulating the subcellular localization of SNF1-RELATED KINASE 1 (SnRK1) in Arabidopsis thaliana. Under normal growth conditions, SnRK1 alpha 1 is localized in the nucleus, promoting cell proliferation and meristem size. However, in response to ABA, SnRK1 alpha 1 translocates to the cytoplasm, leading to the inhibition of TOR and reduced cell proliferation and meristem size. This suggests that the subcellular localization of SnRK1 is a crucial mechanism for plants to respond to environmental changes.
The phytohormone abscisic acid (ABA) promotes plant tolerance to major stresses such as drought, partly by modulating growth through poorly understood mechanisms. Here, we show that ABA-triggered repression of cell proliferation in the Arabidopsis thaliana root meristem relies on the swift subcellular relocalization of SNF1-RELATED KINASE 1 (SnRK1). Under favorable conditions, the SnRK1 catalytic subunit, SnRK1 alpha 1, is enriched in the nuclei of root cells, and this is accompanied by normal cell proliferation and meristem size. Depletion of two key drivers of ABA signaling, SnRK2.2 and SnRK2.3, causes constitutive cytoplasmic localization of SnRK1 alpha 1 and reduced meristem size, suggesting that, under nonstress conditions, SnRK2s promote growth by retaining SnRK1 alpha 1 in the nucleus. In response to ABA, SnRK1 alpha 1 translocates to the cytoplasm, and this is accompanied by inhibition of target of rapamycin (TOR), decreased cell proliferation, and reduced meristem size. Blocking nuclear export with leptomycin B abrogates ABA-driven SnRK1 alpha 1 relocalization to the cytoplasm and ABA-elicited inhibition of TOR. Furthermore, fusing SnRK1 alpha 1 to an SV40 nuclear localization signal leads to defective ABA-dependent TOR repression. Altogether, we demonstrate that SnRK2-dependent changes in SnRK1 alpha 1 subcellular localization are crucial for inhibiting TOR and root growth in response to ABA. Rapid relocalization of central regulators such as SnRK1 may represent a general strategy of eukaryotic organisms to respond to environmental changes.

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