ArticleScientific reports2016
The mitochondrial protease AtFTSH4 safeguards Arabidopsis shoot apical meristem function.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Functional FTSH4 complexes in Arabidopsis mitochondria: a megacomplex with SLP1 and SLP1-free smaller complexes.Plant & cell physiology · 2026Article
- A LTR retrotransposon insertion leads to leafy phenotype in maize by elevating ZmOM66 expression.Nature communications · 2025Article
- A mitochondrial metalloprotease FtsH4 is required for symbiotic nitrogen fixation in Lotus japonicus nodules.Scientific reports · 2024Article
- Robust organ size in Arabidopsis is primarily governed by cell growth rather than cell division patterns.Development (Cambridge, England) · 2024Article
- Genome-wide identification and characterization of filamentation temperature-sensitive H (FtsH) genes and expression analysis in response to multiple stresses in Medicago truncatula.Molecular biology reports · 2023Article
- Robust organ size in Arabidopsis is primarily governed by cell growth rather than cell division patterns.bioRxiv : the preprint server for biology · 2023Article
- Soybean Calmodulin-Binding Transcription Activators, GmCAMTA2 and GmCAMTA8, Coordinate the Circadian Regulation of Developmental Processes and Drought Stress Responses.International journal of molecular sciences · 2023Article
- Transcription factor WOX11 regulates protein translation via ribosome protein acetylation in rice roots.Plant physiology · 2023Article
- Dynamic Changes in Reactive Oxygen Species in the Shoot Apex Contribute to Stem Cell Death inInternational journal of molecular sciences · 2022Article
- Effect of heat stress on oxidative damage and antioxidant defense system in white clover (Trifolium repens L.).Planta · 2021Article
- FTSH4 and OMA1 mitochondrial proteases reduce moderate heat stress-induced protein aggregation.Plant physiology · 2021Article
- Thermopriming-Induced Autophagy in Shoot Apical Meristem of Arabidopsis.Iranian journal of biotechnology · 2021Article
- Lonely at the top? Regulation of shoot apical meristem activity by intrinsic and extrinsic factors.Current opinion in plant biology · 2020Review
- Regulation of Shoot Apical Meristem and Axillary Meristem Development in Plants.International journal of molecular sciences · 2020Review
- Article
- OPENER Is a Nuclear Envelope and Mitochondria Localized Protein Required for Cell Cycle Progression in Arabidopsis.The Plant cell · 2019Article
- Stem cells within the shoot apical meristem: identity, arrangement and communication.Cellular and molecular life sciences : CMLS · 2019Review
- Mechanisms of ROS Regulation of Plant Development and Stress Responses.Frontiers in plant science · 2019Review
- Redox regulation of cell proliferation: Bioinformatics and redox proteomics approaches to identify redox-sensitive cell cycle regulators.Free radical biology & medicine · 2018Review
- Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4.International journal of molecular sciences · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The shoot apical meristem (SAM) ensures continuous plant growth and organogenesis. In LD 30 °C, plants lacking AtFTSH4, an ATP-dependent mitochondrial protease that counteracts accumulation of internal oxidative stress, exhibit a puzzling phenotype of premature SAM termination. We aimed to elucidate the underlying cellular and molecular processes that link AtFTSH4 with SAM arrest. We studied AtFTSH4 expression, internal oxidative stress accumulation, and SAM morphology. Directly in the SAM we analysed H2O2 accumulation, mitochondria behaviour, and identity of stem cells using WUS/CLV3 expression. AtFTSH4 was expressed in proliferating tissues, particularly during the reproductive phase. In the mutant, SAM, in which internal oxidative stress accumulates predominantly at 30 °C, lost its meristematic fate. This process was progressive and stage-specific. Premature meristem termination was associated with an expansion in SAM area, where mitochondria lost their functionality. All these effects destabilised the identity of the stem cells. SAM termination in ftsh4 mutants is caused both by internal oxidative stress accumulation with time/age and by the tissue-specific role of AtFTSH4 around the flowering transition. Maintaining mitochondria functionality within the SAM, dependent on AtFTSH4, is vital to preserving stem cell activity throughout development.
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