Involvement of Arabidopsis BIG protein in cell death mediated by Myo- Inositol homeostasis Article - 2020

Quentin Bruggeman, Florence Piron-Prunier, Frederique Tellier, Jean-Denis Faure, David Latrasse, Deborah Manza-Mianza, Christelle Mazubert, Sylvie Citerne, Stephanie Boutet-Mercey, Raphaël Lugan, Catherine Bergounioux, Cécile Raynaud, Moussa Benhamed, Marianne Delarue

Quentin Bruggeman, Florence Piron-Prunier, Frederique Tellier, Jean-Denis Faure, David Latrasse, Deborah Manza-Mianza, Christelle Mazubert, Sylvie Citerne, Stephanie Boutet-Mercey, Raphaël Lugan, Catherine Bergounioux, Cécile Raynaud, Moussa Benhamed, Marianne Delarue, « Involvement of Arabidopsis BIG protein in cell death mediated by Myo- Inositol homeostasis  », Scientific Reports, à paraître. ISSN 2045-2322

Abstract

Programmed cell death (PCD) is essential for several aspects of plant life. We previously identified the mips1 mutant of Arabidopsis thaliana, which is deficient for the enzyme catalysing myo-inositol synthesis, and that displays light-dependent formation of lesions on leaves due to Salicylic Acid (SA) over-accumulation. Rationale of this work was to identify novel regulators of plant PCD using a genetic approach. A screen for secondary mutations that abolish the mips1 PCD phenotype identified a mutation in the BIG gene, encoding a factor of unknown molecular function that was previously shown to play pleiotropicroles in plant development and defence. Physiologicalanalyses showed that BIG is required for lesion formation in mips1 via SA-dependant signalling. bigmutations partly rescued transcriptomic and metabolomics perturbations as stress-related phytohormones homeostasis. In addition, since loss of function of the ceramide synthase LOH2 was not able to abolish cell death induction in mips1, we show that PCD induction is not fully dependent of sphingolipid accumulation as previously suggested. Our results provide further insights into the role of the BIG protein in the control of MIPS1-dependent cell death and also into the impact of sphingolipid homeostasis in this pathway.

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