Biology subjects

Blanchet, S.

Publications and source records attributed to Blanchet, S..

At least 19 recordsLinked to original sources

bioRxiv2026

A few genes modulate the ecological impact of a freshwater fish species on food webs and ecosystem functions

Genetic diversity within species can shape food webs and ecosystem functioning as strongly as species diversity, yet the genomic architecture underlying these effects remains unclear. Gene-to-ecosystem relationships may arise from genome-wide diversity, from a limited number of ecologically-important genes, or a combination of both. Experimental tests of these hypotheses are lacking. Here, we manipulated genomic diversity of a top-predatory fish in mesocosms under ambient or warm conditions, and quantified ecological responses spanning fish biomass, prey communities and ecosystem functions. Genome-wide diversity explained few ecological responses, with moderate effects (r=0.260). In contrast, variation at specific candidate SNPs predicted all ecological responses consistently across climatic conditions, with effect sizes being more than twice those of genome-wide estimates (r=0.599). Moreover, combining information from small subsets of candidate SNPs outperformed both single-locus and genome-wide diversity for all ecological responses (r=0.841), consistent with an oligogenic architecture for gene-to-ecosystem relationships. Enrichment analyses revealed functional pathways related to growth, development and metabolic regulation, driven by a small set of pleiotropic genes. We demonstrate that the ecological consequences of intraspecific genetic variation arose from a limited fraction of the genome, highlighting the importance of functional genomic structure, rather than genome-wide diversity alone, in shaping eco-evolutionary dynamics.

ecology↗

bioRxiv2026

Warming and predation drive rapid evolution of ecosystem functioning but not functional traits

Global environmental change can rapidly reshape phenotypic trait distributions through adaptive and neutral processes. Yet, disentangling their relative contributions remains a major challenge, particularly for traits underpinning ecosystem functioning. Using a two-year mesocosm study, we experimentally evolved Asellus aquaticus under contrasting temperature and predation regimes to test how the joint influence of these global change pressures shape the evolution of traits and ecosystem functioning. We show that classic functional traits (body size and metabolic rate) showed no evidence of divergent evolution across evolutionary conditions, while ecosystem function itself, namely decomposition rate, has evolved rapidly and differently depending on evolutionary conditions, with the highest decomposition rate observed for Asellus populations exposed to high temperatures in the absence of their predator. A Pst/Fst comparison revealed that divergence in metabolic rate among evolutionary conditions was mainly driven by genetic drift, whereas, for body mass and decomposition rate, non-neutral processes (natural selection and/or plasticity) were also involved, albeit in a different way. By demonstrating that predation and temperature can influence the evolution of an ecosystem function over a few generations, this study represents an important first step toward uncovering the combined effects of global change on the eco-evolutionary dynamics of ecosystems.

evolutionary biology↗

bioRxiv2026

Breast cancer metabolism and responsiveness to dichloroacetate: relationships with 15N and 13C natural abundance

BackgroundMetabolic reprogramming is a hallmark of breast cancer (BrCa), with alterations in glycolysis, glutamine metabolism, and the urea cycle contributing to tumour progression. Dichloroacetate (DCA), a pyruvate dehydrogenase kinase (PDK) inhibitor, shifts metabolism toward oxidative phosphorylation and has been proposed as a therapeutic agent. While isotope tracing is well-established, natural isotope abundance ({delta}{superscript 1}3C, {delta}{superscript 1}N) is emerging as a biomarker of metabolic alterations in cancer. MethodsWe investigated the relationship between isotope composition and metabolism in BrCa using two BALB/c mouse mammary tumour models (V14 and 4T1) and assessed the effects of DCA treatment using metabolomics, lipidomics and isotopomics. ResultsV14 and 4T1 tumours exhibited isotopic patterns similar to human tumours, with {delta}{superscript 1}3C enrichment and {delta}{superscript 1}N depletion relative to non-cancerous mammary tissue. V14 tumours were more {delta}{superscript 1}N-depleted than 4T1, reflecting differences in nitrogen metabolism. Multivariate analysis integrating isotopic, metabolomic, and lipidomic data revealed isotopic features as key discriminators between tumours and normal tissues. Compared to V14, 4T1 tumours were enriched in TCA intermediates, sphingolipids, and amino acids, whereas V14 tumours showed elevated glutaminolytic and nitrogenous metabolites. DCA treatment differentially affected tumour growth, with V14 tumours more sensitive than 4T1. DCA altered nitrogen metabolism, increasing the arginine-to-ornithine ratio, and modulating {delta}{superscript 1}N values in a tumour-specific manner increasing V14 and decreasing 4T1 {delta}{superscript 1}N values. DCA had little effect on {delta}{superscript 1}3C. {delta}{superscript 1}3C values were primarily determined by the balance between lipid and TCA cycle metabolites, rather than glycolytic flux. {delta}{superscript 1}N variation was linked to nitrogen metabolism, including urea cycle intermediates and sphingolipid composition, with a potential role for choline-related fractionation in {delta}{superscript 1}N depletion. Altered gene expression of Hacd2 and Acot12 in V14 tumours after DCA treatment was reflected in shorter fatty acid tails in phosphatidyl cholines, supporting the lipidomics data. ConclusionsThese findings support the hypothesis that cancer-associated metabolic reprogramming influences natural isotope abundance. Correlations between isotope shifts and metabolic signatures highlight the potential of lipid-derived {delta}{superscript 1}N as a biomarker of tumour metabolic state, with implications for noninvasive metabolic profiling in BrCa. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=141 SRC="FIGDIR/small/710495v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@1589d0eorg.highwire.dtl.DTLVardef@af2ad4org.highwire.dtl.DTLVardef@24e67forg.highwire.dtl.DTLVardef@98da7f_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

bioRxiv2026

Environmental RNA improves detection and surveillance of schistosomiasis transmission

Environmental diagnosis of schistosomiasis, a tropical disease affecting more than 250 million people globally, is still challenging, which limits efficient eradication plans. There is a crucial need for resolutive and highly sensitive environmental tools to improve disease control. However, a major obstacle is the inability of current methods, including environmental DNA (eDNA), to distinguish infectious parasite life stages. Here, we develop and validate an environmental RNA (eRNA) approach that enables the detection and absolute quantification of Schistosoma mansoni miracidia and cercariae directly from water samples. After identifying life stage-specific transcripts, we design specific ddPCR assays which are strongly specific to S. mansoni and to each life stage. Comparing with eDNA assays, laboratory experiments demonstrate that stage-specific eRNA assays accurately reflect the relative abundance of each life stage, detect nucleic acids released from organisms, exhibit detection limits tenfold lower than eDNA assays. Also, under laboratory conditions, RNA persists in water longer than DNA. Field validation at six endemic sites in Brazil confirms that eRNA outperforms eDNA and conventional snail surveys in detecting active presence of S. mansoni cercariae, which indicates schistosomiasis transmission risk to humans locally. By enabling active-stage discrimination in environmental monitoring and improving sensitivity (compared to eDNA), our study advances both fundamental understanding and applied surveillance of schistosomiasis transmission, supporting elimination initiatives in affected regions.

ecology↗

bioRxiv2026

KDM7B-mediated demethylation of RNF113A regulates small cell lung cancer sensitivity to alkylation damage

Chemoresistance remains a major obstacle to effective cancer treatment, often driven by enhanced DNA repair mechanisms that enable tumor cells to withstand genotoxic therapies. One such pathway involves the atypical DNA damage repair complex ALKBH3-ASCC, activated by the E3 ligase RNF113A in response to alkylation damage. We previously showed that SMYD3-dependent methylation of RNF113A stimulates this pathway, enhancing DNA repair and promoting resistance. Here, we identify KDM7B/PHF8 as the bona fide RNF113A demethylase, establishing one of the first functional examples of a dynamic, reversible non-histone methylation event regulating genome integrity. KDM7B antagonizes SMYD3 activity by maintaining low levels of methylated RNF113A, thereby limiting ASCC activation and sensitizing cancer cells to alkylating agents. To dissect this regulation in depth, we focused on small cell lung cancer (SCLC), a particularly aggressive malignancy characterized by limited therapeutic options and rapid acquisition of resistance. In SCLC, high KDM7B levels correlate with improved patient prognosis, whereas xenografts with reduced expression exhibit diminished responses to alkylating treatment. Moreover, CRISPR-based on/off modulation of KDM7B in genetically engineered SCLC mouse models demonstrates its central role in determining tumor response to chemotherapy. Our findings position the RNF113A-ASCC axis as a central modulator of chemoresistance, regulated through a post-translational methylation switch representing an innovative therapeutic vulnerability that could be exploited to enhance the efficacy of alkylating agents. Targeting this pathway may provide new opportunities to overcome chemoresistance, with KDM7B levels serving as a predictive biomarker to guide treatment in SCLC.

cell biology↗

bioRxiv2025

High-resolution HIV-1 m6A epitranscriptome reveals splicing-dependent methylation clusters and unique 2-LTR transcript modifications

The N6-methyladenosine (m6A) modification of HIV-1 has been widely studied but the number and precise positions of the m6A sites remain unclear due to the lack of precision of detection methods. Using the latest Nanopore chemistry and direct m6A base-calling, we identified 18 m6A: 14 at the 3 end and 4 in central regions of the genome. Our data reveal differential methylation of these positions between splicing isoforms. Eleven of these sites are clustered in two short segments with peak-shaped methylation profiles. Single-molecule analysis revealed that a very small number of transcripts were unmethylated in both clusters. We also identified a [~]732 nt RNA species resulting from the transcription of non-integrated viral DNA circles closed by two long terminal repeats. These transcripts started in the first LTR, terminated at the polyA site of the second LTR and harbored six m6A sites. Five of these sites were present in other transcripts and, remarkably, had the highest methylation rates. The sixth site was methylated only in this transcript, suggesting a role for this RNA in HIV-1 infection. These findings reveal a new landscape of HIV m6A transcriptome modifications and pave the way for studies deciphering their role in the viral life cycle.

bioinformatics↗

bioRxiv2025

Behavior Outpaces Form when Linking Traits to Ecological Responses within Populations: A Meta-Analysis

Intraspecific variability is fundamental to ecology, yet we still know remarkably little about what governs the strength of the associations between traits expressed by individuals and ecological dynamics. To explore this overlooked aspect of diversity, we asked whether the strength of correlations between traits and a wide spectrum of ecological responses could differ (i) between intraspecific levels (among vs. within populations), (ii) among ecological responses across levels of biological organization (from ecological performance to ecosystem functioning), and (iii) among trait types (morphology, physiology, and behavior). We performed a meta-analysis synthesizing over a thousand effect sizes from nearly two hundred studies spanning approximately a hundred animal species across a broad range of traits and ecological responses. The average effect size was |r| = 0.26 (95% confidence interval: 0.21 - 0.30). At the individual level, effect sizes were larger for ecological performance (foraging, diet) than for fitness (reproduction), and tended to be larger for community responses (e.g., community composition of surrounding organisms). Physiology and behavior showed larger effect sizes than morphology. Our meta-analysis not only confirms that intraspecific trait variability is central to ecological dynamics, but also highlights physiology and behavior as key traits for unraveling the ecological consequences of individual variability.

ecology↗

bioRxiv2024

Early seedling development in dark conditions is directly controlled by plastids through the GUN1-dependent plastid retrograde pathway

In dark growth conditions, seedlings develop specific features such as an elongated hypocotyl, a tightly folded apical hook, and non-green cotyledons. This dark-specific process, known as skotomorphogenesis, relies primarily on mitochondria and eventually etioplasts for energy. Our previous research shows that skotomorphogenesis is reprogrammed in response to mitochondrial and plastidial dysfunction. Even though the direct link between mitochondria and skotomorphogenesis was described, the impact of plastid dysfunction on early development could not be separated from mitochondrial stress. In this study, we aim to determine the direct connection between plastid functionality and skotomorphogenic response. In this situation, we analyze the phenotypic, molecular, and metabolic effects of treating etiolated seedlings using lincomycin and spectinomycin, which target plastid translation. Our results with the lincomycin treatment highlight the direct role of plastids in the control of early development, even in dark growth conditions, in the absence of any photosynthetic activity, and without the involvement of mitochondrial intermediates. Additionally, our findings suggest that GUN1 plays a regulatory role in regulating nuclear gene expression in response to plastid translation inhibition. Thanks to our study, we can now build a more precise model proposing a straight link between the reprogramming of early development and the dysfunction of plastids in dark-growth conditions. Significance statementIn underground germination conditions, seedlings follow a dark-specific development program, called skotomorphogenesis, that is required for their efficient emergence from the soil. Our study demonstrates that plastids play a crucial role in controlling skotomorphogenesis, even in the absence of photosynthetic activity and without affecting mitochondrial function, and therefore we propose that regulation of etioplast functions might contribute to the adaptation of seedling development to constraining environmental conditions.

plant biology↗

bioRxiv2024

Responses of grapevine cells to physiological doses of ethanol, among which induced resistance to heat stress

Grapevine naturally endures stresses like heat, drought, and hypoxia. A recent study showed very low oxygen levels inside grape berries, linked to ethanol content. Other studies have established the link between ethanol and tolerance to various stresses: heat stress, drought, and high salinity. The causes of such a tolerance are not well understood. In our study, three-week-old Gamay calli, Vitis vinifera, were characterised for their endogenous oxygen levels and endogenous ethanol concentration. Subsequently, a transcriptomic study of these cells was conducted, 6 and 24 hours after treatment with 1 mM ethanol. After 6 hours, ethanol addition led to 386 differentially expressed genes, with a notable upregulation of genes related to heat response, especially small Heat Shock Proteins (sHSPs). Further experiments showed that ethanol priming in grape cells or in Arabidopsis seedlings reduced pigment and electrolyte leakage under heat stress, respectively. This study supports the idea that ethanol priming helps protect plants against heat stress and provides a valuable RNA-seq dataset for further research into the underlying mechanisms, sHSPs playing a potentially crucial role in this adaptive response.

plant biology↗

bioRxiv2024

When does a parasite become a disease? eDNA unravels complex host-pathogen dynamics across environmental stress gradients in wild salmonid populations

Infectious diseases stem from disrupted interactions among hosts, parasites, and the environment. Both abiotic and biotic factors can influence infection outcomes by shaping the abundance of a parasites infective stages, as well as the hosts ability to fight infection. However, disentangling these mechanisms within natural ecosystems remains challenging. Here, combining environmental DNA analysis and niche modeling at a regional scale, we uncovered the biotic and abiotic drivers of a lethal infectious disease of salmonid fish, triggered by the parasite Tetracapsuloides bryosalmonae. We found that the occurrence and abundance of the parasite in the water--i.e., the propagule pressure-- were mainly correlated to the abundances of its two primary hosts, the bryozoan Fredericella sultana and the fish Salmo trutta, but poorly to local abiotic environmental stressors. In contrast, the occurrence and abundance of parasites within fish hosts--i.e., proxies for disease emergence--were closely linked to environmental stressors (water temperature, agricultural activities, dams), and to a lesser extent to parasite propagule pressure. These results suggest that pathogen distribution alone cannot predict the risk of disease in wildlife, and that local anthropogenic stressors may play a pivotal role in disease emergence among wild host populations, likely by compromising the hosts ability to fight the parasite. Our study sheds light on the intricate interplay between biotic and abiotic factors in shaping pathogen distribution and raises concerns about the effects of global change on disease emergence.

ecology↗

bioRxiv2024

GENETIC DIVERSITY AFFECTS ECOSYSTEM FUNCTIONS ACROSS TROPHIC LEVELS AS MUCH AS SPECIES DIVERSITY, BUT IN AN OPPOSITE DIRECTION

Understanding the relationships between biodiversity and ecosystem functioning stands as a cornerstone in ecological research. Extensive evidence now underscores the profound impact of species loss on the stability and dynamics of ecosystem functions. However, it remains unclear whether the loss of genetic diversity within key species yield similar consequences. Here, we delve into the intricate relationship between species diversity, genetic diversity, and ecosystem functions across three trophic levels --primary producers, primary consumers, and secondary consumers-- in natural aquatic ecosystems. Our investigation involves estimating species diversity and genome-wide diversity -gauged within three pivotal species-within each trophic level, evaluating seven key ecosystem functions, and analyzing the magnitude of the relationships between biodiversity and ecosystem functions (BEFs). We found that, overall, the absolute effect size of genetic diversity on ecosystem functions mirrors that of species diversity in natural ecosystems. We nonetheless unveil a striking dichotomy: while genetic diversity was positively correlated with various ecosystem functions, species diversity displays a negative correlation with these functions. These intriguing antagonist effects of species and genetic diversity persists across the three trophic levels (underscoring its systemic nature), but were apparent only when BEFs were assessed within trophic levels rather than across them. This study reveals the complexity of predicting the consequences of genetic and species diversity loss under natural conditions, and emphasizes the need for further mechanistic models integrating these two facets of biodiversity.

ecology↗

bioRxiv2023

Cytoskeleton remodeling induced by SMYD2 methyltransferase drives breast cancer metastasis

Malignant forms of breast cancer refractory to existing therapies remain a major unmet health issue, primarily due to metastatic spread. A better understanding of the mechanisms at play will provide better insights for alternative treatments to prevent breast cancer cells dispersion. Here, we identify the lysine methyltransferase SMYD2 as a clinically actionable master regulator of breast cancer metastasis. While SMYD2 is overexpressed in aggressive breast cancers, we notice that it is not required for primary tumor growth. However, mammary-epithelium specific SMYD2 ablation increases mouse overall survival by blocking the primary tumor cells ability to metastasize. Mechanistically, we identify BCAR3 as a genuine physiological substrate of SMYD2 in breast cancer cells. BCAR3 monomethylated at lysine K334 (K334me1) is recognized by a novel methyl-binding domain present in FMNLs proteins. These actin cytoskeleton regulators are recruited at the cell edges by the SMYD2 methylation signaling and modulates lamellipodia properties. Breast cancer cells with impaired BCAR3 methylation loose migration and invasiveness capacity in vitro and are ineffective in promoting metastases in vivo. Remarkably, SMYD2 pharmacologic inhibition efficiently impairs the metastatic spread of breast cancer cells, PDX and aggressive mammary tumors from genetically engineered mice. This study provides a rationale for innovative therapeutic prevention of malignant breast cancer metastatic progression by targeting the SMYD2-BCAR3-FMNL axis.

cancer biology↗

bioRxiv2023

The Ribosome Profiling landscape of yeast reveals a high diversity in pervasive translation

Pervasive translation is a widespread phenomenon that plays an important role in de novo gene birth; however, its underlying mechanisms remain unclear. Based on multiple Ribosome Profiling (Ribo-Seq) datasets, we investigated the RiboSeq landscape of coding and noncoding regions of yeast. Therefore, we developed a representation framework which allows the visual representation and rational classification of the entire diversity of Ribo-Seq signals that could be observed in yeast. We show that if coding regions are restricted to specific areas of the Ribo-Seq landscape, noncoding regions are associated with a wide diversity of translation signals and, conversely, populate the entire yeast Ribo-Seq landscape. Specifically, we reveal that noncoding regions are associated with canonical translation signals, but also with non-canonical ones absent from coding regions, and which appear to be a hallmark of pervasive translation. Notably, we report thousands of translated noncoding ORFs among which, 251 led to detectable products with Mass Spectrometry while being characterized by a wide range of translation specificities. Overall, we show that pervasive translation is not random with noncoding ORF translation signals being consistent across Ribo-Seq experiments. Finally, we show that the translation signal of noncoding ORFs is not explained by features related to the emergence of function, but rather determined by the translation start codon and the codon distribution in their two alternative frames. Overall, our results enable us to propose a topology of the pervasive Ribo-Seq landscape of a species, and open the way to future comparative analyses of this translation landscape under different conditions.

evolutionary biology↗

bioRxiv2021

Barrier mitigation measures trigger the rapid recovery of genetic connectivity in five freshwater fish species

Rivers are heavily fragmented by man-made instream barriers such as dams and weirs. This hyper-fragmentation is a major threat to freshwater biodiversity and restoration policies are now adopted worldwide to mitigate these impacts. However, there is surprisingly little feedback on the efficiency of barrier mitigation measures in restoring riverine connectivity, notably for non-migratory fish species. Here, we implemented a "before-after genetic monitoring" of the restoration of 11 weirs in France using a dedicated genetic index of fragmentation (the FINDEX), with a focus on five fish species from two genera. We found that most obstacles actually had a significant impact on connectivity before restoration, especially the highest and steepest ones, with an overall barrier effect of about 51% of the maximal theoretical impact. Most importantly, we demonstrated for the first time that mitigation measures such as dam removal or fish pass creation significantly and rapidly improved connectivity, with -for some barriers-a complete recovery of the genetic connectivity in less than twelve months. Our study provides a unique and strong proof-of-concept that barrier removal is an efficient strategy to restore riverine connectivity and that molecular tools can provide accurate measures of restoration efficiency within a few months. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=80 SRC="FIGDIR/small/471259v1_ufig1.gif" ALT="Figure 1"> View larger version (17K): org.highwire.dtl.DTLVardef@1b9aa38org.highwire.dtl.DTLVardef@5654daorg.highwire.dtl.DTLVardef@1dceedborg.highwire.dtl.DTLVardef@1c56cd1_HPS_FORMAT_FIGEXP M_FIG C_FIG

ecology↗

bioRxiv2020

eEF3 promotes late stages of tRNA translocation on the ribosome

SummaryIn addition to the conserved translation elongation factors eEF1A and eEF2, fungi require a third essential elongation factor, eEF3. While eEF3 has been implicated in tRNA binding and release at the A and E sites, its exact mechanism of action is unclear. Here we show that eEF3 acts at the mRNA–tRNA translocation step by promoting the dissociation of the tRNA from the E site, but independent of aminoacyl-tRNA recruitment to the A site. Depletion of eEF3 in vivo leads to a general slow-down in translation elongation due to accumulation of ribosomes with an occupied A site. Cryo-EM analysis of ex vivo eEF3-ribosome complexes shows that eEF3 facilitates late steps of translocation by favoring non-rotated ribosomal states as well as by opening the L1 stalk to release the E-site tRNA. Additionally, our analysis provides structural insights into novel translation elongation states, enabling presentation of a revised yeast translation elongation cycle.Competing Interest StatementThe authors have declared no competing interest.View Full Text

molecular biology↗

bioRxiv2020

Intraspecific diversity loss in a predator species alters prey community structure and ecosystem functions

AO_SCPLOWBSTRACTC_SCPLOWLoss in intraspecific diversity can alter ecosystem functions, but the underlying mechanisms are still elusive, and intraspecific biodiversity-ecosystem function relationships (iBEF) have been restrained to primary producers. Here, we manipulated genetic and functional richness of a fish consumer (Phoxinus phoxinus), to test whether iBEF relationships exist in consumer species, and whether they are more likely sustained by genetic or functional richness. We found that both genotypic and functional richness affected ecosystem functioning, either independently or in interaction. Loss in genotypic richness reduced benthic invertebrate diversity consistently across functional richness treatments, whereas it reduced zooplankton diversity only when functional richness was high. Finally, both losses in genotypic and functional richness altered essential functions (e.g. decomposition) through trophic cascades. We concluded that iBEF relationships lead to substantial top-down effects on entire food chains. The loss of genotypic richness impacted ecological properties as much as the loss of functional richness, probably because it sustains "cryptic" functional diversity.

ecology↗

bioRxiv2019

Loss of genetic diversity in wild fish populations reduces biomass stability over time.

Genetic diversity sustains species adaptation. However, it may also support key ecosystems functions and services that can be altered by the worldwide loss of genetic diversity. Here, using long-term wild fish data, we demonstrate that populations with high genetic diversity do not reach higher biomasses than populations with low genetic diversity. Nonetheless, populations with high genetic diversity have much more stable biomasses over recent decades than populations having suffered from genetic erosion, which has implications for the provision of ecosystem services and the risk of population extinction. Our results strengthen the importance of adopting prominent environmental policies to conserve this important biodiversity facet.

ecology↗

bioRxiv2019

Quantifying The Individual Impact Of Artificial Barriers In Freshwaters: A Standardized And Absolute Index Of Genetic Connectivity

Fragmentation by artificial barriers is an important threat to freshwater biodiversity. Mitigating the negative aftermaths of fragmentation is of crucial importance, and it is now essential for environmental managers to benefit from a precise estimate of the individual impact of weirs and dams on river connectivity. Although the indirect monitoring of fragmentation using molecular data constitutes a promising approach, it is plagued with several constraints preventing a standardized and individual quantification of barrier effects. Indeed, observed levels of genetic differentiation depend on both the age of the obstacle and the effective size of the populations it separates, making difficult comparisons of the actual barrier effect of different obstacles. Here, we developed a standardized genetic index of fragmentation (FINDEX), allowing an absolute and independent assessment of the individual effects of obstacles on connectivity. The FINDEX is the standardized ratio (expressed as a percentage) between the observed genetic differentiation between pairs of populations located on either side of an obstacle and the genetic differentiation expected if this obstacle completely prevented gene flow. The expected genetic differentiation is calculated from simulations taking into account two nuisance parameters: the number of generations since barrier creation (the age of the obstacle) and the expected heterozygosity of the targeted populations, a proxy for effective population sizes. Using both simulated and published empirical datasets, we explored and discussed the validity and the limits of the FINDEX. We demonstrated that it allows quantifying genetic effects of fragmentation only from a few generations after barrier creation and provides valid comparisons among populations (or species) of different effective populations sizes and obstacles of different ages. The computation of the FINDEX requires a minimum amount of fieldwork and genotypic data, and solves some of the difficulties inherent to the study of artificial fragmentation in rivers and potentially in other ecosystems. This makes the FINDEX a promising and objective tool for managers aiming at at planning restoration programs and at evaluating the efficiency of these programs.

ecology↗