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Hammoudi, V.

Publications and source records attributed to Hammoudi, V..

2 recordsLinked to original sources

SPPiDDRs: a new gene family in dicot plants involved in DNA-Damage Response

Living organisms must maintain the integrity of their genome, and plants are not exempt. In plants, recognition of DNA damage converges at the transcription factor SOG1, a functional homolog of the animal p53 protein. SOG1 directly controls the expression of hundreds of genes and orchestrates a sophisticated network of signaling pathways termed DNA-damage response (DDR). Only recently, several long non-coding RNA (lncRNA) loci were identified to be upregulated by DNA damage, and only a handful have been confirmed to actively contribute to DDR. In this study, we focused on one locus annotated as lncRNA and found that it is strongly and quickly upregulated upon DNA damage and is a direct target of SOG1. Combining in silico and experimental analyses, we demonstrate that this locus was wrongly annotated as lncRNA and is in fact a gene coding for a short protein that targets peroxisomes. Consequently, we renamed this locus SHORT PEROXISOMAL PROTEIN INDUCED IN DNA-DAMAGE RESPONSE1 (SPPiDDR1). SPPiDDRs are well conserved and present in multiple copies across dicot genomes, with Arabidopsis containing two additional copies, SPPiDDR2 and SPPiDDR3. The AtSPPiDDR paralogs differ on the transcriptional level, SPPiDDR3 being the least active. SPPiDDR1 and SPPiDDR2 are both also induced by salt, a stress treatment known to indirectly induce DNA damage via oxidative stress. We show that these two genes act redundantly and inhibit plant growth in response to salt stress.

molecular biology↗

The protein modifier SUMO is critical for Arabidopsis shoot meristem maintenance at warmer ambient temperatures

Short heat waves (>37{degrees}C) are extremely damaging to non-acclimated plants and their capacity to recover from heat stress is key for their survival. To acclimate, the HEAT SHOCK TRANSCRIPTION FACTOR A1 (HSFA1) subfamily activates a transcriptional response that resolves incurred damages. In contrast, little is known how plants acclimate to sustained non-detrimental warm periods at 27-28{degrees}C. Plants respond to this condition with a thermomorphogenesis response. In addition, HSFA1 is critical for plant survival during these warm periods. We find that SUMO, a protein modification whose conjugate levels rise sharply during acute heat stress in eukaryotes, is critical too for plant longevity during warm periods, in particular for normal shoot meristem development. The known SUMO ligases were not essential to endure these warm periods, alone or in combination. Thermo-lethality was also not seen when plants lacked certain SUMO proteases or when SUMO chain formation was blocked. The SUMO-dependent thermo-resilience was as well independent of the autoimmune phenotype of the SUMO mutants. As acquired thermotolerance was normal in the sumo1/2 knockdown mutant, our data thus reveal a role for SUMO in heat acclimation that differs from HSFA1 and SIZ1. We conclude that SUMO is critical for shoot meristem integrity during warm periods. HighlightThe protein modifier SUMO governs shoot meristem maintenance in Arabidopsis allowing sustained rosette development when plants endure a sustained warm non-detrimental period of 28 degrees Celsius.

plant biology↗