RRC ID |
50416
|
Author |
Yamatani H, Kohzuma K, Nakano M, Takami T, Kato Y, Hayashi Y, Monden Y, Okumoto Y, Abe T, Kumamaru T, Tanaka A, Sakamoto W, Kusaba M.
|
Title |
Impairment of Lhca4, a subunit of LHCI, causes high accumulation of chlorophyll and the stay-green phenotype in rice.
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Journal |
J Exp Bot
|
Abstract |
Chlorophyll is an essential molecule for acquiring light energy during photosynthesis. Mutations that result in chlorophyll retention during leaf senescence are called 'stay-green' mutants. One of the several types of stay-green mutants, Type E, accumulates high levels of chlorophyll in the pre-senescent leaves, resulting in delayed yellowing. We isolated delayed yellowing1-1 (dye1-1), a rice mutant whose yellowing is delayed in the field. dye1-1 accumulated more chlorophyll than the wild-type in the pre-senescent and senescent leaves, but did not retain leaf functionality in the 'senescent green leaves', suggesting that dye1-1 is a Type E stay-green mutant. Positional cloning revealed that DYE1 encodes Lhca4, a subunit of the light-harvesting complex I (LHCI). In dye1-1, amino acid substitution occurs at the location of a highly conserved amino acid residue involved in pigment binding; indeed, a severely impaired structure of the PSI-LHCI super-complex in dye1-1 was observed in a blue native PAGE analysis. Nevertheless, the biomass and carbon assimilation rate of dye1-1 were comparable to those in the wild-type. Interestingly, Lhcb1, a trimeric LHCII protein, was highly accumulated in dye1-1, in the chlorophyll-protein complexes. The high accumulation of LHCII in the LHCI mutant dye1 suggests a novel functional interaction between LHCI and LHCII.
|
Volume |
69(5)
|
Pages |
1027-1035
|
Published |
2018-2-23
|
DOI |
10.1093/jxb/erx468
|
PII |
4785936
|
PMID |
29304198
|
PMC |
PMC6019047
|
MeSH |
Light-Harvesting Protein Complexes
Oryza / genetics*
Oryza / metabolism*
Phenotype
Photosynthesis*
Pigmentation / genetics
Plant Leaves / physiology*
|
IF |
5.908
|
Times Cited |
4
|
Resource |
Rice |
Induced mutation lines |