Detection of adaptive shifts on phylogenies by using shifted stochastic processes on a tree

Comparative and evolutive ecologists are interested in the distribution of quantitative traits between related species. The classical framework for these distributions consists of a random process running along the branches of a phylogenetic tree relating the species. We consider shifts in the process parameters, which reveal fast adaptation to changes of ecological niches. We show that models with shifts are not identifiable in general. Constraining the models to be parsimonious in the number of shifts partially alleviates the problem but several evolutionary scenarios can still provide the same joint distribution for the extant species. We provide a recursive algorithm to enumerate all the equivalent scenarios and to count the number of effectively different scenarios. We introduce an incomplete-data framework and develop a maximum likelihood estimation procedure based on the expectation–maximization algorithm. Finally, we propose a model selection procedure, based on the cardinal of effective scenarios, to estimate the number of shifts and for which we prove an oracle inequality

Inference of Adaptive Shifts for Multivariate Correlated Traits

International audienceTo study the evolution of several quantitative traits, the classical phylogenetic comparative framework consists of a multivariate random process running along the branches of a phylogenetic tree. The Ornstein-Uhlenbeck (OU) process is sometimes preferred to the simple Brownian Motion (BM) as it models stabilizing selection toward an optimum. The optimum for each trait is likely to be changing over the long periods of time spanned by large modern phylogenies. Our goal is to automatically detect the position of these shifts on a phylogenetic tree, while accounting for correlations between traits, which might exist because of structural or evolutionary constraints. We show that, in the presence shifts, phylogenetic Principal Component Analysis (pPCA) fails to decorrelate traits efficiently, so that any method aiming at finding shift needs to deal with correlation simultaneously. We introduce here a simplification of the full multivariate OU model, named scalar OU (scOU), which allows for noncausal correlations and is still computationally tractable. We extend the equivalence between the OU and a BM on a re-scaled tree to our multivariate framework. We describe an Expectation Maximization algorithm that allows for a maximum likelihood estimation of the shift positions, associated with a new model selection criterion, accounting for the identifiability issues for the shift localization on the tree. The method, freely available as an R-package (PhylogeneticEM) is fast, and can deal with missing values. We demonstrate its efficiency and accuracy compared to another state-of-the-art method (l1ou) on a wide range of simulated scenarios, and use this new framework to re-analyze recently gathered datasets on New World Monkeys and Anolis lizards

Multi-Approach Analysis Reveals Local Adaptation in a Widespread Forest Tree of Reunion Island

The nucleotide sequences reported in this article have been submitted to the European Nucleotide Archive under accession numbers SAMEA5423234 to SAMEA5423258 (study no PRJEB31715)International audienceDetecting processes of local adaptation in forest trees andidentifying environmental selective drivers are of primaryimportance for forest management and conservation. Transplant experiments, functional genomics and population genomics are complementary tools to efficiently characterize heritable phenotypic traits and to decipher the genetic bases of adaptive traits. Using an integrative approach combining phenotypic assessment in common garden, transcriptomics and landscape genomics, we investigated leaf adaptive traits in Coffea mauritiana, a forest tree endemic to Reunion Island. Eight populations of C. mauritiana originating from sites with contrasted environmental conditions were sampled in common garden to assessseveral leaf morphological traits, to analyze the leaf transcriptome and leaf cuticular wax composition. The relative alkane content of cuticular waxes was significantly correlated with major climatic gradients, paving the way for further transcriptome-based analyses. The expression pattern of cuticle biosynthetic genes was consistent with a modulation of alkane accumulation across the population studied, supporting the hypothesis that the composition of cuticular wax is involved in the local adaptation of C. mauritiana. Association tests in landscape genomics performed using RNA-seq-derived single-nucleotide polymorphisms revealed that genes associated with cell wall remodeling also likely play an adaptive role. By combining these different approaches, this study efficiently identified local adaptation processes in a non-model species. Our results provide the first evidence for local adaptation in trees endemic to Reunion Island and highlight the importance of cuticle composition for the adaptation of trees to the high evaporative demand in warm climates

Safeguarding the diversity of species of the genus Coffea in Réunion Island

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Bottom-up preparation of MgH 2 nanoparticles with enhanced cycle life stability during electrochemical conversion in Li-ion batteries

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Endospanin-2 enhances skeletal muscle energy metabolism and running endurance capacity.

Metabolic stresses such as dietary energy restriction or physical activity exert beneficial metabolic effects. In the liver, endospanin-1 and endospanin-2 cooperatively modulate calorie restriction-mediated (CR-mediated) liver adaptations by controlling growth hormone sensitivity. Since we found CR to induce endospanin protein expression in skeletal muscle, we investigated their role in this tissue. In vivo and in vitro endospanin-2 triggers ERK phosphorylation in skeletal muscle through an autophagy-dependent pathway. Furthermore, endospanin-2, but not endospanin-1, overexpression decreases muscle mitochondrial ROS production, induces fast-to-slow fiber-type switch, increases skeletal muscle glycogen content, and improves glucose homeostasis, ultimately promoting running endurance capacity. In line, endospanin-2-/- mice display higher lipid peroxidation levels, increased mitochondrial ROS production under mitochondrial stress, decreased ERK phosphorylation, and reduced endurance capacity. In conclusion, our results identify endospanin-2 as a potentially novel player in skeletal muscle metabolism, plasticity, and function

Pancreatology

BACKGROUND: PRSS1 and PRSS2 constitute the only functional copies of a tandemly-arranged five-trypsinogen-gene cluster (i.e., PRSS1, PRSS3P1, PRSS3P2, TRY7 and PRSS2) on chromosome 7q35. Variants in PRSS1 and PRSS2, including missense and copy number variants (CNVs), have been reported to predispose to or protect against chronic pancreatitis (CP). We wondered whether a common trypsinogen pseudogene deletion CNV (that removes two of the three trypsinogen pseudogenes, PRSS3P2 and TRY7) might be associated with CP causation/predisposition. METHODS: We analyzed the common PRSS3P2 and TRY7 deletion CNV in a total of 1536 CP patients and 3506 controls from France, Germany, India and Japan by means of quantitative fluorescent multiplex polymerase chain reaction. RESULTS: We demonstrated that the deletion CNV variant was associated with a protective effect against CP in the French, German and Japanese cohorts whilst a trend toward the same association was noted in the Indian cohort. Meta-analysis under a dominant model yielded a pooled odds ratio (OR) of 0.68 (95% confidence interval (CI) 0.52-0.89; p = 0.005) whereas an allele-based meta-analysis yielded a pooled OR of 0.84 (95% CI 0.77-0.92; p = 0.0001). This protective effect is explicable by reference to the recent finding that the still functional PRSS3P2/TRY7 pseudogene enhancers upregulate pancreatic PRSS2 expression. CONCLUSIONS: The common PRSS3P2 and TRY7 deletion CNV was associated with a reduced risk for CP. This finding provides additional support for the emerging view that dysregulated PRSS2 expression represents a discrete mechanism underlying CP predisposition or protection