Dataset Information

Comparative Proteomics at the Critical Node of Vigor Loss in Wheat Seeds Differing in storability

ABSTRACT: iTRAQ-based comparative proteomic analysis on the critical node of viability loss in wheat seeds with obvious divergence in storability.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Triticum Aestivum (wheat)

TISSUE(S): Plant Cell, Embryo

SUBMITTER: chen xiuling

LAB HEAD: Xinxiong Lu

PROVIDER: PXD025860 | Pride | 2021-09-25

REPOSITORIES: Pride

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Publications

Comparative Proteomics at the Critical Node of Vigor Loss in Wheat Seeds Differing in Storability.

Chen Xiuling X Börner Andreas A Xin Xia X Nagel Manuela M He Juanjuan J Li Jisheng J Li Na N Lu Xinxiong X Yin Guangkun G

Frontiers in plant science 20210830

The critical node (CN, 85% germination) of seed viability is an important threshold for seed regeneration decisions after long-term conservation. Dependent on the germplasm, the storage period until CN is reached varies and information on the divergence of the proteomic profiles is limited. Therefore, the study aims to identify key proteins and mechanisms relevant for a long plateau phase and a late CN during artificial seed aging of wheat. Seeds of the storage-tolerant genotype (ST) TRI 23248, ...[more]

PMID: 34527008

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Project description:This experiment was conducted to identify the mitochondrial protein changes in the presence and absence of LONP1 in skeletal muscle. The following abstract from the submitted manuscript describes the major findings of this work.Disuse-associated loss of muscle LONP1 impairs mitochondrial quality and causes reduced skeletal muscle mass and strength. Zhisheng Xu, Tingting Fu, Qiqi Guo, Danxia Zhou, Wanping Sun, Zheng Zhou, Lin Liu, Liwei Xiao, Yujing Yin, Yuhuan Jia, Xin Pan, Lei Fang, Min-sheng Zhu, Wenyong Fei, Bin Lu and Zhenji Gan. Mitochondrial proteolysis is an evolutionarily conserved quality control mechanism to maintain proper mitochondrial integrity and function. However, the physiological relevance of stress-induced impaired mitochondrial protein quality remains unclear. Here, we demonstrate that LONP1, a major mitochondrial protease resides in the matrix, plays a critical role in controlling mitochondrial quality as well as skeletal muscle mass and strength in response to muscle disuse. In humans and mice, disuse-related muscle loss is associated with decreased mitochondrial LONP1 protein. Skeletal muscle-specific ablation of LONP1 in mice resulted in impaired mitochondrial protein turnover, leading to mitochondrial dysfunction. This caused reduced muscle fiber size and strength. Mechanistically, aberrant accumulation of mitochondrial-retained protein in muscle upon loss of LONP1 induces the activation of autophagy-lysosome degradation program of muscle loss. Overexpressing a mitochondrial-retained mutant ornithine transcarbamylase (ΔOTC), a known protein degraded by LONP1, in skeletal muscle induces mitochondrial dysfunction, autophagy activation, and cause muscle loss and weakness. Thus, these findings reveal a pivotal role of LONP1-dependent mitochondrial protein quality-control in safeguarding mitochondrial function and preserving skeletal muscle mass and strength, and unravel an intriguing link between mitochondrial protein quality and muscle mass maintenance during muscle disuse.

Dataset Information

Comparative Proteomics at the Critical Node of Vigor Loss in Wheat Seeds Differing in storability

Publications

Comparative Proteomics at the Critical Node of Vigor Loss in Wheat Seeds Differing in Storability.

Similar Datasets

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