ES5 is involved in the regulation of phosphatidylserine synthesis and impacts on early senescence in rice (Oryza sativa L.)
Leaf senescence, which affects plant growth and yield in rice, is an ideal target for crop improvement and remarkable advances have been made to identify the mechanism underlying this process. We have characterized an early senile mutant es5 ( e arly leaf s enescence 5 ) in rice exhibiting leaf yell...
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Veröffentlicht in: | Plant molecular biology 2020-03, Vol.102 (4-5), p.501-515 |
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Zusammenfassung: | Leaf senescence, which affects plant growth and yield in rice, is an ideal target for crop improvement and remarkable advances have been made to identify the mechanism underlying this process. We have characterized an early senile mutant
es5
(
e
arly leaf
s
enescence
5
) in rice exhibiting leaf yellowing phenotype after the 4-leaf stage. This phenotype was confirmed by the higher accumulation of reactive oxygen species (ROS) and malondialdehyde (MDA), the disintegration of chloroplasts, reduction in chlorophyll content and photosynthetic rate and up-regulation of senescence-associated genes (SAGs) like
Osh36
,
OsI57
, and
OsI85
. Positional cloning revealed that the
es5
phenotype is the result of one base substitution in
ES5
, encoding phosphatidylserine synthase (PSS) family protein, which is involved in the base-exchange type reaction to synthesize the minor membrane phospholipid phosphatidylserine. Functional complementation of
ES5
in the
es5
plants completely restored the wild-type phenotype. Ultra-high-performance liquid chromatography (UHPLC) analysis showed that
es5
plants had increased levels of phosphatidylserine (PS) and decreased level of phosphatidylcholine (PC). These results provide evidence about the role of PS in rice leaf senescence.
Key message
The
ES5
locus was cloned by map-based cloning that encodes a phosphatidylserine synthase. Mutation in
ES5
caused accumulation of phosphatidylserine which influences premature leaf senescence in rice (
Oryza sativa
L.). |
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ISSN: | 0167-4412 1573-5028 |
DOI: | 10.1007/s11103-019-00961-4 |