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Gonzalo M. Estavillo

Researcher at Commonwealth Scientific and Industrial Research Organisation

Publications -  35
Citations -  3131

Gonzalo M. Estavillo is an academic researcher from Commonwealth Scientific and Industrial Research Organisation. The author has contributed to research in topics: Arabidopsis & Retrograde signaling. The author has an hindex of 20, co-authored 33 publications receiving 2628 citations. Previous affiliations of Gonzalo M. Estavillo include Australian National University & University of Florida.

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The Absence of ALTERNATIVE OXIDASE1a in Arabidopsis Results in Acute Sensitivity to Combined Light and Drought Stress

TL;DR: Results indicate that aox1a plants have a greatly altered stress response even when mitochondria or the mitochondrial electron transport chain are not the primary target of the stress and that AOX1a plays a broad role in determining the normal redox balance in the cell.
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Remodeled Respiration in ndufs4 with Low Phosphorylation Efficiency Suppresses Arabidopsis Germination and Growth and Alters Control of Metabolism at Night

TL;DR: In this paper, the authors characterized an Arabidopsis (Arabidopsis thaliana) mutant, ndufs4 (for NADH dehydrogenase [ubiquinone] fragment S subunit 4), lacking complex I of the respiratory chain, which has constitutively lowered phosphorylation efficiency.
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Signaling from the Endoplasmic Reticulum Activates Brassinosteroid Signaling and Promotes Acclimation to Stress in Arabidopsis

TL;DR: A connection between ER stress signaling and BR-mediated growth and stress acclimation is revealed, suggesting a mechanism by which plants may optimize growth during challenging environmental conditions.

Remodeled Respiration in ndufs4 with Low Phosphorylation Efficiency Suppresses Arabidopsis Germination and Growth and Alters Control of

TL;DR: Insight is provided into how cellular metabolism flexibly adapts to reduced phosphorylation efficiency and why this state may benefit the plant by providing moderate stress tolerance and the data suggest that the absence of complex I alters the adenylate control of cellular metabolism.