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Masiero, S.

Publications and source records attributed to Masiero, S..

3 recordsLinked to original sources

Genomic insights into the virulence repertoire and hemibiotrophic lifestyle of the grapevine black rot pathogen Phyllosticta ampelicida

Phyllosticta ampelicida, the causal agent of grapevine black rot, is a globally emerging pathogen that infects all grapevine green tissues, with young shoots and berries being particularly susceptible. Severe infections can result in total crop loss. To investigate its virulence repertoire, we generated a high-quality genome assembly of strain GW18.1 using long-read sequencing, resulting in 22 scaffolds, including four complete chromosomes and 12 chromosome arms, with a total genome size of 35.6 Mb and 10,289 predicted protein-coding genes. Two additional strains (TN2 and LB22.1) were sequenced with short reads to assess intraspecies diversity. Comparative genomics revealed a conserved virulence factor repertoire, including 314 carbohydrate-active enzymes (CAZymes), 17 cytochrome P450s, 35 peroxidases, and 20 secondary metabolite biosynthetic gene clusters (BGCs). Trophic lifestyle prediction based on gene content supports a biotrophic-like lifestyle consistent with hemibiotrophic pathogens. Broader comparisons with other Phyllosticta species and ten plant-pathogenic fungi pointed to species-specific features, while analysis of gene family evolution identified expansions and contractions in transporters and CAZymes. These genomic resources will support efforts to better understand and manage grapevine black rot.

genomics↗

HISTONE DEACETYLASE 19 REGULATES SHOOT MERISTEMLESS EXPRESSION IN THE CARPEL MARGIN MERISTEM CONTRIBUTING TO OVULE NUMBER DETERMINATION AND TRANSMITTING TRACT DIFFERENTIATION

The gynoecium is critical for the reproduction of flowering species as it contains the ovules and the tissues required for pollen germination and guidance. These tissues are collectively known as the reproductive tract (ReT) and comprise stigma, style and transmitting tract (TT). The ovules and the ReT originate from a meristem within the pistil named carpel margin meristem (CMM). SHOOT MERISTEMLESS (STM) is a key transcription factor required for meristem formation and maintenance. In all above-ground meristems, including the CMM, STM has to be locally downregulated to allow proper organ differentiation. However, how this downregulation is achieved in the CMM is unknown. In this work, we have studied HISTONE DEACETYLASE 19 (HDA19) role in ovule and ReT differentiation, based on the observation that hda19-3 mutant displays reduced ovule number and fails to properly differentiate the TT. Fluorescence activated cell sorting (FACS) coupled with RNA-seq revealed that in the CMM of hda19-3 mutant, genes promoting organ development are downregulated while meristematic markers, including STM, are upregulated. We found that HDA19 is fundamental to downregulate STM in the CMM, allowing ovule formation and TT differentiation. STM is ectopically expressed in hda19-3 at intermediate stages of pistil development, and its downregulation by RNA interference alleviated hda19-3 phenotypic defects. Furthermore, chromatin immunoprecipitation assays indicated that STM is a direct target of HDA19 during pistil development and that SEEDSTICK (STK) is required for the histone acetylation-mediated regulation of STM. Our results have led to the identification of the factors required for STM silencing in the gynoecium allowing organogenesis and tissue differentiation from the CMM.

plant biology↗

Perturbation of protein homeostasis brings plastids at the crossroad between repair and dismantling

The chloroplast proteome is a dynamic mosaic of plastid- and nuclear-encoded proteins. Plastid protein homeostasis is maintained through the balance between de novo synthesis and proteolysis. Intracellular communication pathways, including the plastid-to-nucleus signalling and the protein homeostasis machinery, made of stromal chaperones and proteases, shape chloroplast proteome based on developmental and physiological needs. However, the maintenance of fully functional chloroplasts is costly and under specific stress conditions the degradation of damaged chloroplasts is essential to the maintenance of a healthy population of photosynthesising organelles while promoting nutrient redistribution to sink tissues. In this work, we have addressed this complex regulatory chloroplast- quality-control pathway by modulating the expression of two nuclear genes encoding plastid ribosomal proteins PRPS1 and PRPL4. By transcriptomics, proteomics and transmission electron microscopy analyses, we show that the increased expression of PRPS1 gene leads to chloroplast degradation and early flowering, as an escape strategy from stress. On the contrary, the overaccumulation of PRPL4 protein is kept under control by increasing the amount of plastid chaperones and components of the unfolded protein response (cpUPR) regulatory mechanism. This study advances our understanding of molecular mechanisms underlying chloroplast retrograde communication and provides new insight into cellular responses to impaired plastid protein homeostasis.

plant biology↗