The ABA–AtNAP–SAG113 PP2C module regulates leaf senescence by dephoshorylating SAG114 SnRK3.25 in Arabidopsis
We previously reported that ABA inhibits stomatal closure through AtNAP-SAG113 PP2C regulatory module during leaf senescence. The mechanism by which this module exerts its function is unknown. Here we report the identification and functional analysis of SAG114 , a direct target of the regulatory mod...
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Published in | Molecular horticulture Vol. 3; no. 1; pp. 22 - 13 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
London
Springer Nature B.V
30.10.2023
BioMed Central BMC |
Subjects | |
Online Access | Get full text |
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Summary: | We previously reported that ABA inhibits stomatal closure through AtNAP-SAG113 PP2C regulatory module during leaf senescence. The mechanism by which this module exerts its function is unknown. Here we report the identification and functional analysis of
SAG114
, a direct target of the regulatory module.
SAG114
encodes SnRK3.25. Both bimolecular fluorescence complementation (BiFC) and yeast two-hybrid assays show that SAG113 PP2C physically interacts with SAG114 SnRK3.25. Biochemically the SAG113 PP2C dephosphorylates SAG114 in vitro and
in planta
. RT-PCR and GUS reporter analyses show that
SAG114
is specifically expressed in senescing leaves in Arabidopsis. Functionally, the SAG114 knockout mutant plants have a significantly bigger stomatal aperture and a much faster water loss rate in senescing leaves than those of wild type, and display a precocious senescence phenotype. The premature senescence phenotype of
sag114
is epistatic to
sag113
(that exhibits a remarkable delay in leaf senescence) because the
sag113 sag114
double mutant plants show an early leaf senescence phenotype, similar to that of
sag114
. These results not only demonstrate that the ABA-AtNAP-SAG113 PP2C regulatory module controls leaf longevity by dephosphorylating SAG114 kinase, but also reveal the involvement of the SnRK3 family gene in stomatal movement and water loss during leaf senescence.
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 2730-9401 2730-9401 |
DOI: | 10.1186/s43897-023-00072-1 |