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Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4.

ABSTRACT: Shoot and root apical meristems (SAM and RAM, respectively) are crucial to provide cells for growth and organogenesis and therefore need to be maintained throughout the life of a plant. However, plants lacking the mitochondrial protease AtFTSH4 exhibit an intriguing phenotype of precocious cessation of growth at both the shoot and root apices when grown at elevated temperatures. This is due to the accumulation of internal oxidative stress and progressive mitochondria dysfunction. To explore the impacts of the internal oxidative stress on SAM and RAM functioning, we study the expression of selected meristem-specific (STM, CLV3, WOX5) and cell cycle-related (e.g., CYCB1, CYCD3;1) genes at the level of the promoter activity and/or transcript abundance in wild-type and loss-of-function ftsh4-1 mutant plants grown at 30 °C. In addition, we monitor cell cycle progression directly in apical meristems and analyze the responsiveness of SAM and RAM to plant hormones. We show that growth arrest in the ftsh4-1 mutant is caused by cell cycle dysregulation in addition to the loss of stem cell identity. Both the SAM and RAM gradually lose their proliferative activity, but with different timing relative to CYCB1 transcriptional activity (a marker of G2-M transition), which cannot be compensated by exogenous hormones.

SUBMITTER: Dolzblasz A

PROVIDER: S-EPMC5877714 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

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Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4.

Dolzblasz Alicja A Gola Edyta M EM Sokołowska Katarzyna K Smakowska-Luzan Elwira E Twardawska Adriana A Janska Hanna H

International journal of molecular sciences 20180314 3

Shoot and root apical meristems (SAM and RAM, respectively) are crucial to provide cells for growth and organogenesis and therefore need to be maintained throughout the life of a plant. However, plants lacking the mitochondrial protease AtFTSH4 exhibit an intriguing phenotype of precocious cessation of growth at both the shoot and root apices when grown at elevated temperatures. This is due to the accumulation of internal oxidative stress and progressive mitochondria dysfunction. To explore the ...[more]

PMID: 29538317

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Project description:The peptidase ClpP is conserved from bacteria to human. In the mitochondrial matrix, it multimerizes and forms a macromolecular proteasome-like cylinder. Because of its known relevance for the mitochondrial unfolded protein response during cell stress, we characterized two ClpP knock-out mouse founder lines and documented similar phenotypes. Ubiquitously, ClpP absence led to accumulation of its interactor protein ClpX without transcript upregulation. Interestingly, most wild-type tissues with substantial ClpP amounts had no detectable ClpX. This inverse correlation suggests that ClpX levels and degradation are regulated by ClpP. The expectation of similar protein levels, in view of a reported association of heptameric ClpP rings with hexameric ClpX rings, was confirmed only in testis of wild-type animals. Germline tissue was exceptional also in its vulnerability to ClpP deletion, with both founder lines showing complete infertility for males and females. Otherwise, ubiquitous mitochondrial dysfunction was apparent from severe growth retardation and reduced spontaneous motor activity of the animals, and from a pronounced decrease in pre-/postnatal survival. Spermatogenesis was found aborted at the spermatid stage, acrosomes and axonemes were not formed. Overall, tissue-specific roles of ClpP were evident by this massive effect for germ cells, mild bioenergetic deficits in muscle and liver tissues, and excellent compensation in brain. ClpX was previously reported to chaperone unfolded proteins and also DNA condensation in mitochondria, so it is likely that this pathway is particularly susceptible in germ cells. In conclusion, our study indicates that the role of ClpP in quality control is indispensable during development for cells with rapid changes of mitochondrial numbers, and is relevant during aging for growth and survival of the organism. Factorial design comparing ClpP knock-out mice with wild type littermates in five different tissues (brain, testis, liver, skeletal and heart muscle)

Dataset Information

Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4.

Publications

Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4.

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