Maize yields over Europe may increase in spite of climate change, with an appropriate use of the genetic variability of flowering time

Projections based on invariant genotypes and agronomic practices indicate that climate change will largely decrease crop yields. The comparatively few studies considering farmers’ adaptation result in a diversity of impacts depending on their assumptions. We combined experiments and process-based modeling for analyzing the consequences of climate change on European maize yields if farmers made the best use of the current genetic variability of cycle duration, based on practices they currently use. We first showed that the genetic variability of maize flowering time is sufficient for identifying a cycle duration that maximizes yield in a range of European climatic conditions. This was observed in six field experiments with a panel of 121 accessions and extended to 59 European sites over 36 years with a crop model. The assumption that farmers use optimal cycle duration and sowing date was supported by comparison with historical data. Simulations were then carried out for 2050 with 3 million combinations of crop cycle durations, climate scenarios, management practices, and modeling hypotheses. Simulated grain production over Europe in 2050 was stable (−1 to +1%) compared with the 1975–2010 baseline period under the hypotheses of unchanged cycle duration, whereas it was increased (+4–7%) when crop cycle duration and sowing dates were optimized in each local environment. The combined effects of climate change and farmer adaptation reduced the yield gradient between south and north of Europe and increased European maize production if farmers continued to make the best use of the genetic variability of crop cycle duration

Identification of orthologous regions associated with tissue growth under water-limited conditions

Plant recovery from early season drought is related to the amount of biomass retained during stress and biomass production after the end of stress. Reduction in leaf expansion is one of the first responses to water deficit. It is assumed that the control of tissue development under water deficit contributes to traits such as early vigor, as well as maintenance of growth of reproductive organs. To dissect the underlying mechanisms controlling tissue expansion under water-limited conditions, we used a multilevel approach combining quantitative genetics and genomics. To identify orthologous genetic regions controlling tissue growth under water-limited conditions a series of QTL mapping and microarray gene expression studies were conducted in rice and maize. Results of differentially expressed genes from microarray experiments, QTLs and candidate genes related to growth in the different species are compared on consensus maps (within species) and then on synteny maps (between species), to identify common genetic regions between rice and maize

Physiological and genetic control of transpiration efficiency in African rice, Oryza glaberrima Steud

Improving crop water use efficiency, the amount of carbon assimilated as biomass per unit of water used by a plant, is of major importance as water for agriculture becomes scarcer. In rice, the genetic bases of transpiration efficiency, the derivation of water use efficiency at the whole-plant scale, and its putative component trait transpiration restriction under high evaporative demand remain unknown. These traits were measured in 2019 in a panel of 147 African rice (Oryza glaberrima) genotypes known to be potential sources of tolerance genes to biotic and abiotic stresses. Our results reveal that higher transpiration efficiency is associated with transpiration restriction in African rice. Detailed measurements in a subset of highly contrasted genotypes in terms of biomass accumulation and transpiration confirmed these associations and suggested that root to shoot ratio played an important role in transpiration restriction. Genome wide association studies identified marker-trait associations for transpiration response to evaporative demand, transpiration efficiency, and its residuals, with links to genes involved in water transport and cell wall patterning. Our data suggest that root-shoot partitioning is an important component of transpiration restriction that has a positive effect on transpiration efficiency in African rice. Both traits are heritable and define targets for breeding rice with improved water use strategies.This work was supported by the Institut de Recherche pour le Développement, the CGIAR Research Program (CRP) on rice-agrifood systems (RICE, 2017-2022) and the Agence Nationale de la Recherche (grant ANR-17-MPGA-0011 to VV). Financial support by the Access to Research Infrastructures activity in the Horizon 2020 Programme of the EU (EPPN2020 Grant Agreement 731013) is gratefully acknowledged. PA was supported by a doctoral fellowship from the French Ministry of Higher Education. BEE was supported by the Centre National de la Recherche Scientifique et Technologique of Gabon. The authors acknowledge the IRD iTrop HPC (South Green Platform) at IRD Montpellier for providing HPC resources (https://bioinfo.ird.fr, http://www.southgreen.fr)

Filling the gaps in gene banks: collecting, characterizing and phenotyping wild banana relatives of Papua New Guinea

International audienceSince natural habitats are disappearing fast, there is an urgent need to collect, characterize, and phenotype banana (Musa spp.) crop wild relatives to identify unique genotypes with specific traits that fill the gaps in our gene banks. We report on a collection mission in Papua New Guinea carried out in 2019. Seed containing bunches were collected from Musa peekelii ssp. angustigemma (N.W.Simmonds) Argent (3), M. schizocarpa N. W. Simmonds (4), M. balbisiana Colla (3), M. acuminata ssp. banksii (F. Muell.) Simmonds (14), M. boman Argent (3), M. ingens Simmonds (2), M. maclayi ssp. maclayi F.Muell. ex Mikl.-Maclay (1), and M. lolodensis Cheesman (1). This material, together with the seeds collected during a previous mission in 2017, form the basis for the development of a wild banana seed bank. For characterization and phenotyping, we focused on the most ubiquitous indigenous species of Papua New Guinea: M. acuminata ssp. banksii, the ancestor of most edible bananas. We calculated that the median genomic dissimilarity of the M. acuminata ssp. banksii accessions was 4% and that they differed at least 5% from accessions present in the International Transit Centre, the world's largest banana gene bank. High-throughput phenotyping revealed drought avoidance strategies with significant differences in root/shoot ratio, soil water content sensitivity, and response towards vapor pressure deficit (VPD). We deliver a proof of principle that the wild diversity is not yet fully covered in the gene banks and that wild M. acuminata ssp. banksii populations contain individuals with unique traits, useful for drought tolerance breeding programs

Cell cycle-specific UNG2 phosphorylations regulate protein turnover, activity and association with RPA

Human UNG2 is a multifunctional glycosylase that removes uracil near replication forks and in non-replicating DNA, and is important for affinity maturation of antibodies in B cells. How these diverse functions are regulated remains obscure. Here, we report three new phosphoforms of the non-catalytic domain that confer distinct functional properties to UNG2. These are apparently generated by cyclin-dependent kinases through stepwise phosphorylation of S23, T60 and S64 in the cell cycle. Phosphorylation of S23 in late G1/early S confers increased association with replication protein A (RPA) and replicating chromatin and markedly increases the catalytic turnover of UNG2. Conversely, progressive phosphorylation of T60 and S64 throughout S phase mediates reduced binding to RPA and flag UNG2 for breakdown in G2 by forming a cyclin E/c-myc-like phosphodegron. The enhanced catalytic turnover of UNG2 p-S23 likely optimises the protein to excise uracil along with rapidly moving replication forks. Our findings may aid further studies of how UNG2 initiates mutagenic rather than repair processing of activation-induced deaminase-generated uracil at Ig loci in B cells

Mechanisms of c-Myc Degradation by Nickel Compounds and Hypoxia

Nickel (Ni) compounds have been found to cause cancer in humans and animal models and to transform cells in culture. At least part of this effect is mediated by stabilization of hypoxia inducible factor (HIF1a) and activating its downstream signaling. Recent studies reported that hypoxia signaling might either antagonize or enhance c-myc activity depending on cell context. We investigated the effect of nickel on c-myc levels, and demonstrated that nickel, hypoxia, and other hypoxia mimetics degraded c-myc protein in a number of cancer cells (A549, MCF-7, MDA-453, and BT-474). The degradation of the c-Myc protein was mediated by the 26S proteosome. Interestingly, knockdown of both HIF-1α and HIF-2α attenuated c-Myc degradation induced by Nickel and hypoxia, suggesting the functional HIF-1α and HIF-2α was required for c-myc degradation. Further studies revealed two potential pathways mediated nickel and hypoxia induced c-myc degradation. Phosphorylation of c-myc at T58 was significantly increased in cells exposed to nickel or hypoxia, leading to increased ubiquitination through Fbw7 ubiquitin ligase. In addition, nickel and hypoxia exposure decreased USP28, a c-myc de-ubiquitinating enzyme, contributing to a higher steady state level of c-myc ubiquitination and promoting c-myc degradation. Furthermore, the reduction of USP28 protein by hypoxia signaling is due to both protein degradation and transcriptional repression. Nickel and hypoxia exposure significantly increased the levels of dimethylated H3 lysine 9 at the USP28 promoter and repressed its expression. Our study demonstrated that Nickel and hypoxia exposure increased c-myc T58 phosphorylation and decreased USP28 protein levels in cancer cells, which both lead to enhanced c-myc ubiquitination and proteasomal degradation

Duration of female parental care and their survival in the little auk Alle alle - are these two traits linked?

Desertion of offspring before its independence by one of the parents is observed in a number of avian species with bi-parental care but reasons for this strategy are not fully understood. This behaviour is particularly intriguing in species where bi-parental care is crucial to raise the brood successfully. Here, we focus on the little auk, Alle alle, a small seabird with intensive bi-parental care, where the female deserts the brood at the end of the chick rearing period. The little auk example is interesting as most hypotheses to explain desertion of the brood by females (e.g. “re-mating hypothesis”, “body condition hypothesis”) have been rejected for this species. Here, we analysed a possible relationship between the duration of female parental care over the chick and her chances to survive to the next breeding season. We performed the study in two breeding colonies on Spitsbergen with different foraging conditions – more favourable in Hornsund and less favourable in Magdalenefjorden. We predicted that in Hornsund females would stay for shorter periods of time with the brood and would have higher survival rates in comparison with birds from Magdalenefjorden. We found that indeed in less favourable conditions of Magdalenefjorden, females stay longer with the brood than in the more favourable conditions of Hornsund. Moreover, female survival was negatively affected by the length of stay in the brood. Nevertheless, duration of female parental care over the chick was not related to their parental efforts, earlier in the chick rearing period, and survival of males and females was similar. Thus, although females brood desertion and winter survival are linked, the relationship is not straightforward

sel-11 and cdc-42, Two Negative Modulators of LIN-12/Notch Activity in C. elegans

Background: LIN-12/Notch signaling is important for cell-cell interactions during development, and mutations resulting in constitutive LIN-12/Notch signaling can cause cancer. Loss of negative regulators of lin-12/Notch activity has the potential for influencing cell fate decisions during development and the genesis or aggressiveness of cancer. Methodology/Principal Findings: We describe two negative modulators of lin-12 activity in C. elegans. One gene, sel-11, was initially defined as a suppressor of a lin-12 hypomorphic allele; the other gene, cdc-42, is a well-studied Rho GTPase. Here, we show that SEL-11 corresponds to yeast Hrd1p and mammalian Synoviolin. We also show that cdc-42 has the genetic properties consistent with negative regulation of lin-12 activity during vulval precursor cell fate specification. Conclusions/Significance: Our results underscore the multiplicity of negative regulatory mechanisms that impact on lin-12/ Notch activity and suggest novel mechanisms by which constitutive lin-12/Notch activity might be exacerbated in cancer