Réponses à long terme des stocks d'azote du sol selon la rotation et la source de nutriments utilisées en production laitière au Québec

Tableau d’honneur de la Faculté des études supérieures et postdoctorales, 2018-2019.L’utilisation de lisier à des fins de fertilisation est une pratique courante des systèmes de production laitière du Québec et représente une alternative intéressante aux fertilisants minéraux en offrant une source d’azote disponible aux plantes et de matière organique pour le sol. Les objectifs de ce projet situé au nord du lac Saint-Jean (Normandin, Qc) étaient d’évaluer les changements à long terme (21 ans) des stocks de N dans le profil du sol (0-50 cm) selon deux rotations de cultures (céréales continues ou rotation céréale - plantes fourragères pérennes), combinées à deux types de travail du sol primaire (chisel ou charrue à versoirs) et à deux sources de nutriments (minéral ou lisier de bovins) et de dresser le bilan des flux d’azote dans le système sol-plante, pour les systèmes culturaux comparés. L’apport annuel et répété sur 21 ans de lisier de bovins a augmenté les stocks d’azote en surface (0-20 cm) de 14 %, comparativement à la fertilisation minérale, mais n’a montré aucun effet en dessous de 20 cm. La rotation comportant des plantes pérennes a favorisé également une plus grande accumulation (+ 25 %) d’azote dans le sol pour l’horizon 0-20 cm que la monoculture d’orge. La combinaison d’un apport de lisier au système de cultures en rotation avec plantes pérennes a montré un effet bénéfique encore plus important, avec des stocks d’azote du sol supérieurs de 32 % par rapport au système de céréales continues avec lisier (+2,04 t N ha-1 sur le profil entier [0-50 cm]). Le type de travail du sol n’a pas eu d’impact significatif sur les stocks d’azote du profil du sol entier (0-50 cm). Une approche de défaut de bilan entrées-sorties suggère que la présence de légumineuses dans le mélange fourrager contribue à augmenter considérablement les stocks d’azote du sol

Selection of rhizobial strains differing in their nodulation kinetics under low temperature in four temperate legume species

Abstract Background Winter climate change including frequent freeze‐thaw episodes and shallow snow cover will have major impacts on the spring regrowth of perennial crops. Non‐bloating perennial forage legume species including sainfoin, birdsfoot trefoil, red clover, and alsike clover have been bred for their adaptation to harsh winter conditions. In parallel, the selection of cold‐tolerant rhizobial strains could allow earlier symbiotic nitrogen (N) fixation to hasten spring regrowth of legumes. Methods To identify strains forming nodules rapidly and showing high N‐fixing potential, 60 rhizobial strains in association with four temperate legume species were evaluated over 11 weeks under spring soil temperatures for kinetics of nodule formation, nitrogenase activity, and host yield. Results Strains differed in their capacity to form efficient nodules on legume hosts over time. Strains showing higher nitrogenase activity were arctic strain N10 with sainfoin and strain L2 with birdsfoot trefoil. For clovers, nitrogenase activity was similar for control and inoculated plants, likely due to formation of effective nodules in controls by endophyte rhizobia present in seeds. Conclusions Selection based on nodulation kinetics at low temperature, nitrogenase activity, and yield was effective to identify performant rhizobial strains for legume crops. The use of cold‐tolerant strains could help mitigate winter climatic changes

Rare Copy Number Variants Contribute to Congenital Left-Sided Heart Disease

<div><p>Left-sided congenital heart disease (CHD) encompasses a spectrum of malformations that range from bicuspid aortic valve to hypoplastic left heart syndrome. It contributes significantly to infant mortality and has serious implications in adult cardiology. Although left-sided CHD is known to be highly heritable, the underlying genetic determinants are largely unidentified. In this study, we sought to determine the impact of structural genomic variation on left-sided CHD and compared multiplex families (464 individuals with 174 affecteds (37.5%) in 59 multiplex families and 8 trios) to 1,582 well-phenotyped controls. 73 unique inherited or de novo CNVs in 54 individuals were identified in the left-sided CHD cohort. After stringent filtering, our gene inventory reveals 25 new candidates for LS-CHD pathogenesis, such as <em>SMC1A</em>, <em>MFAP4</em>, and <em>CTHRC1</em>, and overlaps with several known syndromic loci. Conservative estimation examining the overlap of the prioritized gene content with CNVs present only in affected individuals in our cohort implies a strong effect for unique CNVs in at least 10% of left-sided CHD cases. Enrichment testing of gene content in all identified CNVs showed a significant association with angiogenesis. In this first family-based CNV study of left-sided CHD, we found that both co-segregating and <em>de novo</em> events associate with disease in a complex fashion at structural genomic level. Often viewed as an anatomically circumscript disease, a subset of left-sided CHD may in fact reflect more general genetic perturbations of angiogenesis and/or vascular biology.</p> </div

Karyotype der(9)ins(X;9)(p11.22;q12) in family 5.

<p>(a,b) FISH was performed on metaphase chromosomes obtained from peripheral blood with a labeled BAC clone that mapped within the detected copy gain (RP11-52N6, red) and a control probe mapped to the Xp/Yp pseudoautosomal region of the sex chromosomes (DXYS129 & DXYS153, green). Green dots show the control probe hybridized to the p arm of chromosomes X and Y. Red dots show the RP11-52N6 BAC clone hybridized on chromosome X (white arrow heads) and in the heterochromatin of chromosome 9 (white arrows). A star shows the normal chromosome 9. These results show that the copy gain is due to a der(9)ins(X;9)(p11.22;q12) in both the father (a) and his son (b). (c). Chromosomal region of the insertion (X;9)(p11.22;q12) in the father and the son of family 5. Four RefSeq genes are identified within this <i>region IQSEC2, RIBC2, HSD17B10</i> and the Cornelia de Lange gene <i>SMC1A</i>. One larger and one smaller CNV have been detected in the DGV database in this region.</p

Identified candidate genes.

<p>Compilation of the 25 LS-CHD candidate genes fulfilling all selection criteria. From left to right: gene name; ENDEAVOUR <i>in silico</i> prioritization; fold overexpression in SAGE experiments outflow tract versus atria/ventricles; <i>in situ</i> hybridization in mouse hearts at embryonic day E10.5; transmission pattern (individual IDs); genomic location.</p

mRNA expression profile of <i>CTHRC1</i> and <i>MFAP4</i> in embryonic mouse heart.

<p>(a, b). <i>In situ</i> hybridizations for <i>MFAP4</i> of a sagittal section of a wild-type stage E 14.5 mouse heart (c, d) <i>In situ</i> hybridizations for <i>CTHRC1</i> of a sagittal section of a wild-type stage E 14.5 mouse heart. Both assays show a strong expression in the pulmonary valve (arrows) and aortic/mitral valve (arrowheads). Unlike <i>CTHRC1</i> which is more restricted to the valves and only weakly expressed in the endothelium of the aorta, <i>MFAP4</i> shows a strong expression in the pulmonary artery and ascending aorta (asterisks). Pictures are taken from Eurexpress (<a href="http://www.eurexpress.org" target="_blank">www.eurexpress.org</a>).</p

dup(4)(p16.1) in family 43.

<p>FISH was performed on metaphase chromosomes and nuclei obtained from peripheral blood with a labeled BAC clone mapped within the detected copy gain (RP11-89K12, green) and a control probe mapped to 4p14 (RP11-332F10, red). (a) Two series of adjacent green dots show the extra copy of the duplicated segment on chromosome 4. (b) The nucleus view with the three green dots showing three copies of the region overlapping the Ellis van Creveld genes on chromosome 4 (c) Log 2 ratio for the large gain in Family 43 on chromosome 4. In general, dots are scattered around 0 along the x-axis for, whereas the identified gain leads to a clear upward shift (d) Heatmap of the identified gain on chromosome 4, each line refers to one individual. An orange row indicates two copies of the region whereas an extra copy leads to a gain in the intensity (yellow line for the individual in family 43).</p