Effect of grape maturity on the carbohydrate composition of red sparkling wines

Póster presentado en el 10th International Symposium of Enology (OENO 2015), celebrado en Burdeos del 19 de junio al 1 de julio de 2015.The authors thank the INIA for financing this study through the projects RTA2012-00092-C02-01 (with FEDER funds). Leticia Martínez thanks the Consejería de Educación del Gobierno de La Rioja for the FPI-CAR grant.Peer Reviewe

Changes in analytical and volatile compositions of red wines induced by pre-fermentation heat treatment of grapes

Experiments were carried out on Grenache, Carignan and Fer grapes in order to characterize the changes in nitrogen content of the musts, conventional enological parameters and aroma compounds of the wines induced by pre-fermentation heating of the grapes followed by alcoholic fermentation in liquid phase or in solid phase. In comparison to a standard vinification, we showed that a two-hour heat treatment at 70 °C induced a significant loss in several grape-derived aroma compounds (terpenols, norisoprenoids and some phenols) associated with an increase in a-terpineol, guaiacol and 2,6-dimethoxyphenol, which suggests thermal degradation. A significant increase in most of the ethyl esters, in acetates and in fatty acids were observed in wines fermented in liquid phase, together with a decrease in fusel alcohols. The substantial modification in the amino acid composition of the must seems to be a crucial element for the understanding of these changes. Chemical compounds studied in this article: ß-Damascenone (PubChem CID: 5374527); ß-Ionone (PubChem CID: 638014); ß-Citronellol (PubChem CID: 8842); a-Terpineol (PubChem CID: 17100); Linalool (PubChem CID: 6549); 4-Mercapto-4-methyl-2-pentanone (PubChem CID: 88290); 3-Mercaptohexanol (PubChem CID: 521348); 2-Furfurylthiol (PubChem CID: 7363); 3-Isobutyl-2-methoxypyrazine (PubChem CID: 32594); Guaiacol (PubChem CID: 460

Front Microbiol

Brettanomyces bruxellensis is the main spoilage microbial agent in red wines. The use of fungal chitosan has been authorized since 2009 as a curative treatment to eliminate this yeast in conventional wines and in 2018 in organic wines. As this species is known to exhibit great genetic and phenotypic diversity, we examined whether all the strains responded the same way to chitosan treatment. A collection of 53 strains of was used. In the conditions of the reference test, all were at least temporarily affected by the addition of chitosan to wine, with significant decrease of cultivable population. Some (41%) were very sensitive and no cultivable yeast was detected in wine or lees after 3 days of treatment, while others (13%) were tolerant and, after a slight drop in cultivability, resumed growth between 3 and 10 days and remained able to produce spoilage compounds. There were also many strains with intermediate behavior. The strain behavior was only partially linked to the strain genetic group. This behavior was little modulated by the physiological state of the strain or the dose of chitosan used (within the limits of the authorized doses). On the other hand, for a given strain, the sensitivity to chitosan treatment was modulated by the chitosan used and by the properties of the wine in which the treatment was carried out.Recherches sur l’origine et les effets secondaires des propriétés stabilisantes du chitosane fongique dans le vi

SRSF1 Haploinsufficiency Is Responsible for a Syndromic Developmental Disorder Associated with Intellectual Disability

SRSF1 (also known as ASF/SF2) is a non-small nuclear ribonucleoprotein (non-snRNP) that belongs to the arginine/serine (R/S) domain family. It recognizes and binds to mRNA, regulating both constitutive and alternative splicing. The complete loss of this proto-oncogene in mice is embryonically lethal. Through international data sharing, we identified 17 individuals (10 females and 7 males) with a neurodevelopmental disorder (NDD) with heterozygous germline SRSF1 variants, mostly de novo, including three frameshift variants, three nonsense variants, seven missense variants, and two microdeletions within region 17q22 encompassing SRSF1. Only in one family, the de novo origin could not be established. All individuals featured a recurrent phenotype including developmental delay and intellectual disability (DD/ID), hypotonia, neurobehavioral problems, with variable skeletal (66.7%) and cardiac (46%) anomalies. To investigate the functional consequences of SRSF1 variants, we performed in silico structural modeling, developed an in vivo splicing assay in Drosophila, and carried out episignature analysis in blood-derived DNA from affected individuals. We found that all loss-of-function and 5 out of 7 missense variants were pathogenic, leading to a loss of SRSF1 splicing activity in Drosophila, correlating with a detectable and specific DNA methylation episignature. In addition, our orthogonal in silico, in vivo, and epigenetics analyses enabled the separation of clearly pathogenic missense variants from those with uncertain significance. Overall, these results indicated that haploinsufficiency of SRSF1 is responsible for a syndromic NDD with ID due to a partial loss of SRSF1-mediated splicing activity

SRSF1 Haploinsufficiency Is Responsible for a Syndromic Developmental Disorder Associated With Intellectual Disability

SRSF1 (also known as ASF/SF2) is a non-small nuclear ribonucleoprotein (non-snRNP) that belongs to the arginine/serine (R/S) domain family. It recognizes and binds to mRNA, regulating both constitutive and alternative splicing. The complete loss of this proto-oncogene in mice is embryonically lethal. Through international data sharing, we identified 17 individuals (10 females and 7 males) with a neurodevelopmental disorder (NDD) with heterozygous germline SRSF1 variants, mostly de novo, including three frameshift variants, three nonsense variants, seven missense variants, and two microdeletions within region 17q22 encompassing SRSF1. Only in one family, the de novo origin could not be established. All individuals featured a recurrent phenotype including developmental delay and intellectual disability (DD/ID), hypotonia, neurobehavioral problems, with variable skeletal (66.7%) and cardiac (46%) anomalies. To investigate the functional consequences of SRSF1 variants, we performed in silico structural modeling, developed an in vivo splicing assay in Drosophila, and carried out episignature analysis in blood-derived DNA from affected individuals. We found that all loss-of-function and 5 out of 7 missense variants were pathogenic, leading to a loss of SRSF1 splicing activity in Drosophila, correlating with a detectable and specific DNA methylation episignature. In addition, our orthogonal in silico, in vivo, and epigenetics analyses enabled the separation of clearly pathogenic missense variants from those with uncertain significance. Overall, these results indicated that haploinsufficiency of SRSF1 is responsible for a syndromic NDD with ID due to a partial loss of SRSF1-mediated splicing activity

Staphylococcus aureus infective endocarditis versus bacteremia strains: Subtle genetic differences at stake

AbstractInfective endocarditis (IE)(1) is a severe condition complicating 10–25% of Staphylococcus aureus bacteremia. Although host-related IE risk factors have been identified, the involvement of bacterial features in IE complication is still unclear. We characterized strictly defined IE and bacteremia isolates and searched for discriminant features. S. aureus isolates causing community-acquired, definite native-valve IE (n=72) and bacteremia (n=54) were collected prospectively as part of a French multicenter cohort. Phenotypic traits previously reported or hypothesized to be involved in staphylococcal IE pathogenesis were tested. In parallel, the genotypic profiles of all isolates, obtained by microarray, were analyzed by discriminant analysis of principal components (DAPC)(2). No significant difference was observed between IE and bacteremia strains, regarding either phenotypic or genotypic univariate analyses. However, the multivariate statistical tool DAPC, applied on microarray data, segregated IE and bacteremia isolates: IE isolates were correctly reassigned as such in 80.6% of the cases (C-statistic 0.83, P<0.001). The performance of this model was confirmed with an independent French collection IE and bacteremia isolates (78.8% reassignment, C-statistic 0.65, P<0.01). Finally, a simple linear discriminant function based on a subset of 8 genetic markers retained valuable performance both in study collection (86.1%, P<0.001) and in the independent validation collection (81.8%, P<0.01). We here show that community-acquired IE and bacteremia S. aureus isolates are genetically distinct based on subtle combinations of genetic markers. This finding provides the proof of concept that bacterial characteristics may contribute to the occurrence of IE in patients with S. aureus bacteremia

PTX3 Polymorphisms and Invasive Mold Infections After Solid Organ Transplant

Donor PTX3 polymorphisms were shown to influence the risk of invasive aspergillosis among hematopoietic stem cell transplant recipients. Here, we show that PTX3 polymorphisms are independent risk factors for invasive mold infections among 1101 solid organ transplant recipients, thereby strengthening their role in mold infection pathogenesis and patients' risk stratificatio

Role of polysaccharides in wines

International audienc