The OsABCI7 Transporter Interacts with OsHCF222 to Stabilize the Thylakoid Membrane in Rice

He, Yan; Shí, Yùzhēn; Zhang, Xiaobo; Xu, Xiaoqing; Wang, Huimei; Li, Liangjian; Shang, Huihui; Wang, Zhonghao; Wu, Jianli

doi:10.1104/pp.20.00445

Cited by 33 publications

(18 citation statements)

References 60 publications

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“…Total proteins were extracted according to the method of He et al (2020). Antibodies against photosystem proteins (anti-Lhca1, anti-Lhca2, anti-Lhca3, anti-Lhca4, anti-PsbD, and anti-AtpA) were obtained from Agrisera.…”

Section: Protein Analysismentioning

confidence: 99%

Disruption of EARLY LESION LEAF 1, encoding a cytochrome P450 monooxygenase, induces ROS accumulation and cell death in rice

et al. 2020

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Lesion-mimic mutants (LMMs) provide a valuable tool to reveal the molecular mechanisms determining programmed cell death (PCD) in plants. Despite intensive research, the mechanisms behind PCD and the formation of lesions in various LMMs still remain to be elucidated. Here, we identified a rice (Oryza sativa) LMM, early lesion leaf 1 (ell1), cloned the causal gene by map-based cloning, and verified this by complementation. ELL1 encodes a cytochrome P450 monooxygenase, and the ELL1 protein was located in the endoplasmic reticulum. The ell1 mutant exhibited decreased chlorophyll contents, serious chloroplast degradation, upregulated expression of chloroplast degradation-related genes, and attenuated photosynthetic protein activity, indicating that ELL1 is involved in chloroplast development. RNA sequencing analysis showed that genes related to oxygen binding were differentially expressed in ell1 and wild-type plants; histochemistry and paraffin sectioning results indicated that hydrogen peroxide (H 2 O 2) and callose accumulated in the ell1 leaves, and the cell structure around the lesions was severely damaged, which indicated that reactive oxygen species (ROS) accumulated and cell death occurred in the mutant. TUNEL staining and comet experiments revealed that severe DNA degradation and abnormal PCD occurred in the ell1 mutants, which implied that excessive ROS accumulation may induce DNA damage and ROS-mediated cell death in the mutant. Additionally, lesion initiation in the ell1 mutant was light dependent and temperature sensitive. Our findings revealed that ELL1 affects chloroplast development or function, and that loss of ELL1 function induces ROS accumulation and lesion formation in rice.

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Section: Protein Analysismentioning

confidence: 99%

Disruption of EARLY LESION LEAF 1, encoding a cytochrome P450 monooxygenase, induces ROS accumulation and cell death in rice

et al. 2020

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“…2 a, c). Hydrogen peroxide (H 2 O 2 ) over-accumulation is shown to induce plant cell death (He et al 2020 ; Sathe et al 2019 ). We hence detected H 2 O 2 accumulation and cell death of psl50 seedlings with and without heat treatment by using 3,3′-diaminobenzidine (DAB) and trypan blue staining.…”

Section: Resultsmentioning

confidence: 99%

PREMATURE SENESCENCE LEAF 50 Promotes Heat Stress Tolerance in Rice (Oryza sativa L.)

Zhang

Shí

et al. 2021

Rice

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Background Heat stress is a major environmental factor that could induce premature leaf senescence in plants. So far, a few rice premature senescent leaf mutants have been reported to involve in heat tolerance. Findings We identified a premature senescence leaf 50 (psl50) mutant that exhibited a higher heat susceptibility with decreased survival rate, over-accumulated hydrogen peroxide (H2O2) content and increased cell death under heat stress compared with the wild-type. The causal gene PREMATURE SENESCENCE LEAF 50 (PSL50) was isolated by using initial map-based resequencing (IMBR) approach, and we found that PSL50 promoted heat tolerance probably by acting as a modulator of H2O2 signaling in response to heat stress in rice (Oryza sativa L.). Conclusions PSL50 negatively regulates heat-induced premature leaf senescence in rice.

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“…2a, c). Hydrogen peroxide (H 2 O 2 ) over-accumulation is shown to induce plant cell death (He et al 2020;Sathe et al 2019). We hence detected H 2 O 2 accumulation and cell death of psl50 seedlings with and without heat treatment by using 3,3'-diaminobenzidine (DAB) and trypan blue staining.…”

Section: Resultsmentioning

confidence: 99%

Premature Senescence Leaf 50 Promotes Heat Stress Tolerance in Rice (Oryza Sativa L.)

Zhang

Shí

et al. 2020

Preprint

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BackgroundHeat stress is a major environmental factor that could induce premature leaf senescence in plants. So far, few rice premature senescent leaf mutants have been reported to involve in heat tolerance.FindingsWe identified a premature senescence leaf 50 (psl50) mutant that exhibited a higher heat susceptibility with decreased survival rate, over-accumulated hydrogen peroxide (H2O2) content and increased cell death under heat stress compared with the wild-type. The causal gene PREMATURE SENESCENCE LEAF 50 (PSL50) was isolated by using initial map-based resequencing (IMBR) approach, and we found that PSL50 promoted heat tolerance probably by acting as a modulator of H2O2 signaling in response to heat stress in rice (Oryza sativa L.).ConclusionsPSL50 negatively regulates heat-induced premature leaf senescence in rice.

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The OsABCI7 Transporter Interacts with OsHCF222 to Stabilize the Thylakoid Membrane in Rice

Abstract: The OsABCI7 transporter interacts with OsHCF222 at thylakoid membranes to regulate reactive oxygen species homeostasis, thereby maintaining thylakoid membrane stability.

Cited by 33 publications

References 60 publications

Disruption of EARLY LESION LEAF 1, encoding a cytochrome P450 monooxygenase, induces ROS accumulation and cell death in rice

Disruption of EARLY LESION LEAF 1, encoding a cytochrome P450 monooxygenase, induces ROS accumulation and cell death in rice

PREMATURE SENESCENCE LEAF 50 Promotes Heat Stress Tolerance in Rice (Oryza sativa L.)

Premature Senescence Leaf 50 Promotes Heat Stress Tolerance in Rice (Oryza Sativa L.)

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