Role of mitochondrial calcium transport and redox metabolism on dark-induced senescence and aluminum stress tolerance

• Ano de defesa: 2024
• Autor(a) principal: Silva, Marcelle Ferreira
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: eng
• Instituição de defesa: Universidade Federal de Viçosa
• Palavras-chave em Português: Plantas - Efeito do aluminio; Plantas - Efeito da luz; Celulas - Envelhecimento; Estress oxidativo; Calcio - Metabolismo; Mitocrôndia - Metabolismo; Fisiologia Vegetal
• Link de acesso: https://locus.ufv.br/handle/123456789/32490; https://doi.org/10.47328/ufvbbt.2024.429

Stress can be caused by a broad range of conditions and different cellular responses can significantly alter plant metabolism to cope with such conditions. Aluminum (Al) toxicity is a critical factor limiting plant growth in acidic soils. Al is a highly redox reactive element, and its main symptom is root growth inhibition. Dark is another common stress that affects plants; in this scenario, dark-induced senescence is a highly regulated process that requires massive transcriptional and metabolic reprogramming to break down and remobilize valuable resources. For both stresses aforementioned, mitochondrial metabolism is crucial to support cellular processes; accordingly, in Al toxicity it is involved in providing organic acids (OA) to complex Al, whereas in dark conditions it is intimately related to carbon and nitrogen remobilization. In this context, two main processes, related to mitochondria, underpin important cellular responses to these different abiotic stress conditions namely (i) redox system and (ii) calcium (Ca 2+ ) transients. Evidence suggests that thioredoxin (TRX) system are responsible for mitigating oxidative damage through the control of reactive oxygen species (ROS), thus making it important to sustain plant development following abiotic stress. Moreover, Ca 2+ signaling is directly involved in responses to environmental cues. Here we attempted to understand how the Arabidopsis’ mitochondrial TRX system participates in the mitigation of the Al toxicity and how mitochondrial Ca 2+ transporters modulate the dark-induced senescence responses. Surprisingly, our findings revealed the major importance of the GR redox system status in Al mitigation compared to the TRX system. Our results further demonstrated a clear difference in chlorophyll degradation pathway under dark conditions for the mutants lacking the mitochondrial Ca 2+ transporter. We further asked whether this phenomenon was related to the matrix enzyme glutamate dehydrogenase (GDH2) and its regulation by Ca 2+ ; nevertheless, a clear connection between the mitochondrial Ca 2+ transporter and matrix Ca levels and the chlorophyll degradation was not unequivocally apparent. Collectively, our results indicate that mitochondrial metabolism plays an important role in coping with abiotic stress conditions and perturbations in this organelle lead to differential metabolic response under stress conditions. Keywords: Glutamate dehydrogenase; Glutathione; Thioredoxin.