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Biology subjects

Maddalena, G.

Publications and source records attributed to Maddalena, G..

2 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↗

Placental gene expression mediates the interaction between obstetrical history and genetic risk for schizophrenia

Defining the environmental context in which genes enhance susceptibility can provide insight into the pathogenesis of complex disorders, like schizophrenia. Here we show that the intrauterine and perinatal environment modulates the association of schizophrenia with genomic risk, as measured with polygenic risk scores (PRS) based primarily on GWAS significant variants. Genomic risk interacts with intrauterine and perinatal complications (Early Life Complications, ELCs) in each of three independent samples from USA, Italy and Germany (overall n= 1693, p= 6e-05). In each sample, the liability of schizophrenia explained by PRS is nominally more than five times greater in the presence of a history of ELCs compared with its absence. In each sample, patients with positive ELC histories have higher PRS than patients without ELCs, which is further confirmed in two additional patient samples from Germany and Japan (overall n=2038, p= 1e-04). The gene set based on the schizophrenia loci interacting with ELCs is highly expressed in multiple placental compartments and dynamically regulated in placenta from complicated in comparison with normal pregnancies. The same genes are differentially up-regulated in placentae from male compared with female offspring. The interaction between genomic risk and ELCs is mainly driven by GWAS significant loci enriched for genes highly expressed in the various placenta samples. Molecular pathway analyses based on the genes not driving this interaction reflect previous analyses about schizophrenia risk-genes, while genes highly and differentially expressed in placentae implicate an orthogonal biology involving cellular stress. These results suggest that the most significant genetic variants detected by current schizophrenia GWAS contribute to risk in part by converging on a developmental trajectory sensitive to events affecting placentation, which may underlie the male preponderance of schizophrenia and offer new insights into primary prevention.

genetics↗