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Details

Autor(en) / Beteiligte
Titel
Snf1‐related protein kinases SnRK2.4 and SnRK2.10 are involved in maintenance of root system architecture during salt stress
Ist Teil von
  • The Plant journal : for cell and molecular biology, 2012-11, Vol.72 (3), p.436-449
Ort / Verlag
Oxford, UK: Blackwell Publishing Ltd
Erscheinungsjahr
2012
Quelle
MEDLINE
Beschreibungen/Notizen
  • The sucrose non‐fermenting‐1‐related protein kinase 2 (SnRK2) family represents a unique family of plant‐specific protein kinases implicated in cellular signalling in response to osmotic stress. In our studies, we observed that two class 1 SnRK2 kinases, SnRK2.4 and SnRK2.10, are rapidly and transiently activated in Arabidopsis roots after exposure to salt. Under saline conditions, snrk2.4 knockout mutants had a reduced primary root length, while snrk2.10 mutants exhibited a reduction in the number of lateral roots. The reduced lateral root density was found to be a combinatory effect of a decrease in the number of lateral root primordia and an increase in the number of arrested lateral root primordia. The phenotypes were in agreement with the observed expression patterns of genomic yellow fluorescent protein (YFP) fusions of SnRK2.10 and ‐2.4, under control of their native promoter sequences. SnRK2.10 was found to be expressed in the vascular tissue at the base of a developing lateral root, whereas SnRK2.4 was expressed throughout the root, with higher expression in the vascular system. Salt stress triggered a rapid re‐localization of SnRK2.4–YFP from the cytosol to punctate structures in root epidermal cells. Differential centrifugation experiments of isolated Arabidopsis root proteins confirmed recruitment of endogenous SnRK2.4/2.10 to membranes upon exposure to salt, supporting their observed binding affinity for the phospholipid phosphatidic acid. Together, our results reveal a role for SnRK2.4 and ‐2.10 in root growth and architecture in saline conditions.
Sprache
Englisch
Identifikatoren
ISSN: 0960-7412
eISSN: 1365-313X
DOI: 10.1111/j.1365-313X.2012.05089.x
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3533798

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