Biology subjects

Gomez, D.

Publications and source records attributed to Gomez, D..

At least 19 recordsLinked to original sources

bioRxiv2026

DLGAP5 promotes vascular cell proliferation and remodeling in pulmonary arterial hypertension

Background: Pulmonary arterial hypertension (PAH) manifests by pulmonary vascular remodeling, caused by hyper-proliferation and apoptosis resistance of resident PA cells, elevated right ventricular (RV) afterload, and death of RV failure. The goal of this study is to determine the role and mechanisms of action of mitotic spindle-associated microtubule regulator DLG associated protein 5 (DLGAP5) in pulmonary vascular remodeling in PAH. Methods: DLGAP5 expression was assessed in human PAH transcriptomic datasets, PAH patients' lung tissues, pulmonary artery smooth muscle cells (PASMCs), and pulmonary artery adventitial fibroblasts (PAAFs). Loss-of-function, molecular, functional, RNAseq, and network analyses were performed. Smooth muscle (SM)-specific DLGAP5 knockdown using adeno-associated virus serotype 6 (AAV6) in mice with SU5416/hypoxia-induced PH was performed. Results: DLGAP5 was overaccumulated in small muscular PAs, PASMCs, and PAAFs from PAH lungs. siRNA DLGAP5 down-regulated cyclin A2, suppressed hyper-proliferation, increased pro-apoptotic BIM, and induced apoptosis in human PAH PASMCs and PAAFs. DEP domain containing 1 (DEPDC1) was identified and validated as a downstream effector of DLGAP5 in PAH PASMCs responsible for hyper-proliferation and apoptosis resistance of human PAH PASMCs. SM-specific DLGAP5 knockdown with AAV6-enTagln-shDLGAP5 reversed DEPDC1 overaccumulation in small muscular PAs, reduced PA medial thickness, RV systolic pressure, mean PA pressure, and RV hypertrophy in mice with SuHx-induced PH. Conclusions: DLGAP5 supports proliferation and survival of human PAH PASMCs and PAAFs through up-regulation of cyclin A2, DEPDC1, and suppression of BIM, and promotes PA remodeling and PH in mice. DLGAP5 could serve as a potential molecular target to attenuate pulmonary vascular remodeling in PAH.

cell biology↗

bioRxiv2026

CASC15 dictates vascular smooth muscle cell growth fate and pathological vascular remodeling through post-transcription regulation of mitotic fidelity

Vascular smooth muscle cell (SMC) growth, whether hyperplastic or hypertrophic, is a central determinant of vascular remodeling in cardiovascular disease, yet the molecular regulators that direct SMC toward a specific growth fate remain poorly understood. Here, we identify the long non-coding RNA CASC15 as a critical regulator of SMC growth and vascular remodeling. CASC15 is enriched in the vasculature and SMC-rich tissues in humans and mice, and its locus harbors SNPs significantly associated with coronary artery disease and blood pressure. We identify a novel SMC-selective CASC15 isoform (S-CASC15) whose expression level determines SMC growth fate: elevated S-CASC15 promotes proliferation, while its loss drives hypertrophy, polyploidization, and binucleation. In vivo depletion of CASC15 limits vascular injury-induced neointima formation and atherosclerotic lesion expansion. Conversely, CASC15 overexpression exacerbates injury-induced neointimal hyperplasia. However, CASC15 KO mice exhibit spontaneous medial hypertrophy and vascular hypercontractility. Mechanistically, loss of S-CASC15 expression causes mitotic defects, followed by arrest in the G1 phase of hypertrophic and polyploid cells. We found that S-CASC15 pro-proliferative function is mediated through its interaction with RNA-binding proteins, including Nucleolin, and by regulating the stability of cell cycle checkpoint gene transcripts, thereby ensuring mitotic fidelity. Together, these findings establish CASC15 as a pivotal molecular switch governing the balance between hyperplastic and hypertrophic vascular remodeling and as a potential therapeutic target in cardiovascular disease.

Cell Biology↗

bioRxiv2026

Short-term oxycodone exposure produces delayed and persistent gut microbiome disruption in mice

The gut microbiome is a critical part of host homeostasis, yet its resilience following opioid exposure remains poorly understood. While opioid-induced short-term dysbiosis is well documented, the long-term recovery dynamics following oxycodone remain unclear. This study characterized the temporal dynamics of the fecal microbiota in male C57BL/6J mice following a brief 3-day oxycodone regimen (5mg/kg, BID). 16S rRNA gene sequencing was performed at baseline, day 3, 10, 17, and 70. While acute post-treatment phases (day 3 to 10) showed subtle taxonomic shifts in Clostridium_sensu_stricto_1 and Romboutsia, significant community disruption emerged later. By day 17, beta diversity significantly differed from saline controls (P =0.002). At day 70, both alpha diversity (p=0.02) and beta diversity (P=0.007) remained significantly altered, characterized by enriched Akkermansia and Marvinbryantia alongside depleted Eubacterium_xylanophilum. These findings demonstrate that even brief oxycodone exposure triggers persistent, non-recovering dysbiosis that became detectable only after treatment cessation and persisted through day 70. This suggests that the window for microbiome recovery exceeds two months in mice (equivalent to several human years), highlighting a potential long-term risk for patients prescribed short-term opioid courses. ImportanceShort-term opioid exposure is generally assumed to cause only transient disruption of the gut microbiome. However, the duration of microbiome recovery following clinically relevant opioid treatment remains poorly defined. In this study, we show that a brief three-day course of oxycodone in mice resulted in delayed and persistent alterations in gut microbial community structure that remained detectable for at least 70 days after treatment cessation. Notably, significant divergence in microbial composition emerged weeks after exposure rather than immediately following treatment, suggesting that short-term opioid use may initiate longer-lasting remodeling of the gut microbiome than previously appreciated. These findings highlight the importance of considering extended recovery timelines when evaluating the microbiological consequences of opioid exposure.

microbiology↗

bioRxiv2026

Exploiting HSD17B11-dependent dialkynylcarbinols cytotoxicity for facile CRISPR/Cas9-based gene inactivation

Several approaches have been developed to improve the efficiency of CRISPR/Cas9-based genome editing, including the co-inactivation of a gene whose loss confers resistance to a cytotoxic compound, thereby enabling enrichment of successfully edited cells. Here, we show across multiple cell lines that inactivation of HSD17B11, a non-essential member of the Short-chain Dehydrogenase/Reductase (SDR) superfamily, confers strong resistance (29- to 131-fold) to a Phenyl diAlkynylCarbinol compound (PAC) in both human and mouse cells, without affecting cell viability or proliferation. We demonstrate that co-inactivation of HSD17B11 followed by PAC selection can be used to rapidly identify efficient guide RNAs targeting a gene of interest and to readily isolate clones inactivated for one or multiple genes. Altogether, these results establish a simple and efficient experimental strategy for generating knockout cells by using PAC selection to enrich for successfully edited cells.

molecular biology↗

bioRxiv2026

NITRITE INCREASES MITOFUSIN-1 LEVELS TO INHIBIT VASCULAR SMOOTH MUSCLE CELL PROLIFERATION AND PREVENT INTIMAL HYPERPLASIA

Vascular disease remains a leading cause of morbidity and mortality and is driven by maladaptive vascular remodeling following injury. Stent-induced vascular injury induces vascular smooth muscle cell (VSMC) phenotypic switching from a contractile to a proliferative state, resulting in intimal hyperplasia (IH), restenosis and compromised vessel function. Nitrite, an endogenous oxidation product of nitric oxide and a dietary constituent, attenuates IH after vascular injury; however, its underlying mechanisms remain incompletely understood. Nitrite is known to modulate mitochondrial structure and function, and dysregulated mitochondrial dynamics have independently been implicated in VSMC proliferation. We therefore hypothesized that nitrite attenuates IH by modulating mitochondrial dynamics to suppress VSMC proliferation. Using rat aortic smooth muscle cells (RASMCs), we demonstrate that nitrite treatment inhibits cell cycle progression and cell proliferation through upregulation of mitofusin-1 (Mfn1), a GTPase that catalyzes mitochondrial fusion. Mechanistically, nitrite increased Mfn1 protein levels by inhibiting Mfn1 proteasomal degradation. Mfn1 deletion resulted in enhanced proliferation, loss of contractile gene expression, and decreased expression of antioxidant enzymes including catalase and glutathione peroxidase. Restoration of cellular antioxidant capacity significantly attenuated proliferation and preserved contractile gene expression in Mfn1-deficient cells. Smooth muscle cell-specific Mfn1 knockout mice subjected to carotid artery ligation injury exhibited exacerbated IH compared to wildtype mice. Nitrite administration significantly decreased IH in wildtype mice but not Mfn1-deficient mice. These findings identify endogenous Mfn1 as a critical regulator of VSMC cell cycle progression and as an essential mediator of the vasoprotective effects of nitrite.

cell biology↗

bioRxiv2026

Selective Disruption of Plasmodium falciparum mitochondrial DNA via G-Quadruplex-Binding Ligand RHPS4 Provides a Novel Antimalarial Strategy

Malaria caused by Plasmodium falciparum remains a major health threat, killing over 600,000 people annually. The spread of resistance to all major antimalarials, including artemisinins, highlights the urgent need for new drugs with distinct mechanisms of action. Here we show that the G-quadruplex ligand RHPS4, an acridine derivative, displays strong antiplasmodial activity against both drug-sensitive and -resistant P. falciparum strains and clinical isolates. RHPS4 primarily targets the trophozoite stage and induces major mitochondrial alterations, including reduction of mitochondrial DNA (mtDNA) and transcriptional dysfunctions. Bioinformatic analyses identified at least eight putative G4-forming sequences within the parasites mtDNA. Biophysical studies confirmed G4 folding of at least one sequence and its interaction with RHPS4. These findings indicate that RHPS4 disrupts P. falciparum mitochondrial metabolism through G4 stabilization, leading to parasite death, and establish mtDNA G4 structures as novel therapeutic targets for antimalarial development.

microbiology↗

bioRxiv2025

Representations in the hippocampal-entorhinal system emerge from learning sensory predictions

The hippocampal formation and adjacent parahippocampal areas are central to intelligent behaviour such as memory and navigation. Understanding how systems in the brain generate structured representations from experience remains a fundamental goal in neuroscience. A central open question is whether a single computational principle can account for the diverse neural responses observed across the hippocampal-entorhinal circuit. Existing models often rely on hand-crafted features or specialized learning mechanisms unrelated to sensory observations, and typically express representations of only a small subset of known cell types. Further, representations learned in such models are often not empirically evaluated against neural representations observed in the navigating brain. Here, we introduce a neurobiologically-inspired and robust computational model in which diverse cell types emerge from a single learning objective with minimal hand-engineered assumptions. Our model applies contrastive graph representation learning to transitions between high-dimensional visual observations, constructing a metric space in which temporally adjacent sensory observations are mapped to nearby states. Inspired by the anatomical information flow of the hippocampal-entorhinal system, and anchored in output representations based on neural coding in the entorhinal cortex, the model gives rise to activity resembling place cells, grid cells, boundary vector cells, band cells, corner cells, and conjunctive cells among others. Across varied environments and sensory streams, the framework captures not only diverse neural response patterns but also the functional dependencies between them, mirroring the proposed sequential representational structure observed in the hippocampal-entorhinal system. Crucially, place-cell-like features of the model quantitatively reproduce remapping dynamics observed in CA1 of freely moving animals, and afford theoretical explanatory power of existing neurobiologically-informed models. This work thus offers a unified computational model of spatial coding in the hippocampal-entorhinal system and a testable framework for generating mechanistic hypotheses in silico, to be evaluated in vivo.

neuroscience↗

bioRxiv2025

Integrated histopathologic modeling of detailed tumor subtypes and actionable biomarkers

Accurate cancer subtyping with accompanying molecular characterization is critical for precision oncology. While machine learning approaches have been applied to both digital pathology and cancer genomics, previous work has been limited in sample size and has typically aggregated granular cancer subtypes into coarse groupings, likely obfuscating informative molecular and prognostic associations and phenotypic variation of more detailed tumor subtypes. Accordingly, we collated 378,123 hematoxylin and eosin (H&E)-stained whole-slide images (WSIs) with matched targeted DNA clinical sequencing results and OncoTree detailed cancer subtypes from a real-world cohort of 71,142 patients. Using this scaled, granular dataset and a cancer subtype knowledge graph, we developed Mosaic: a family of calibrated machine learning models using H&E WSI embeddings to classify tumors and identify molecular phenotypes across 163 detailed subtypes. The cancer subtyping module (Aeon) achieved an area under the receiver operating characteristic curve (AUROC) of 0.992 overall, with 161/163 subtypes reaching an AUROC [≥] 0.90 and improved performance over a state-of-the-art genomics-based classifier. The genomic inference module (Paladin) achieved an AUROC [≥] 0.80 for 167 pairs of detailed subtypes and genomic targets. We further used the learned histopathologic representations to i) identify key associations of the histopathologic embeddings with clinical biomarkers; ii) identify unsupervised sub-clusters of tumors with genomic determinants of tumor phenotype; iii) specify granular diagnoses for cancers of unknown primary, evaluated by genomic associations and expected clinical outcome distributions; iv) annotate functional significance for variants of uncertain significance (VUS); and v) identify cases that mimic the phenotypic effect of known DNA variants on H&E in the absence of detectable DNA alterations. Taken together, this work advances our understanding of phenotypic variation of granular tumor subtypes, their relevance to enhanced diagnostics, and their potential utility in risk stratification with multimodal machine learning in cancer.

cancer biology↗

bioRxiv2025

Shotgun metagenomic analysis of the oral microbiomes of children with noma reveals a novel disease-associated organism

Noma is a rapidly progressive orofacial gangrene that predominantly affects children living in extreme poverty. Despite its documentation since antiquity and its designation as a World Health Organisation Neglected Tropical Disease in 2023, the microbiological cause of noma remains poorly understood, with no specific organisms confidently identified as definitive aetiological agents. Here, we present the first deep shotgun metagenomic profiling of oral saliva microbiomes from 19 Nigerian children with acute noma. Our analyses reveal marked microbial dysbiosis in noma microbiomes, with machine learning and multivariate statistical analyses indicating significant enrichment of Treponema, Porphyromonas, and Bacteroides, alongside depletion of Streptococcus and Rothia, as key microbial signatures of noma disease. From the dataset we recovered 40 high-quality Treponema metagenome-assembled genomes (MAGs) spanning 19 species, 14 of which were novel. Notably, a novel species designated Treponema sp. A was detected in 15 of the 19 noma participants and was entirely absent from global healthy saliva metagenomes. Re-analysis of previously published 16S rRNA datasets from children with noma in Niger also revealed Treponema sp. A to be highly prevalent in noma cases but rare in controls. This study identifies Treponema--particularly Treponema sp. A--as a strong candidate organism associated with noma pathogenesis. Additionally, analysis of antimicrobial resistance determinants detected in noma metagenomes revealed concerning levels of resistance to antibiotics commonly used in noma treatment, particularly {beta}-lactams and metronidazole, especially among Prevotella species. These findings provide the first high-resolution microbial framework for noma and offer a foundation for future research into its pathogenesis and the development of novel diagnostics, therapeutics, and preventive strategies in endemic settings.

pathology↗

bioRxiv2025

Antibody targeting the anti-parallel topology of human telomeric G-quadruplex DNA

G-quadruplexes (G4s) are four-stranded nucleic acid structures that have gathered a significant attention due to their involvement in key biological processes, including gene regulation, genome stability, and telomeres maintenance. Some G4 antibodies have been developed to selectively recognize these structures over duplex DNA; however, most, even the widely studied BG4 and 1H6, bind G4s in a general manner and lack discrimination between distinct topologies, particularly between parallel and antiparallel conformations. In this study, we report on the development and characterization of a novel antibody selected via phage display method using a constrained antiparallel G4 structure mimicking one of the conformation adopted in vitro by the human telomeric sequence. Our findings demonstrate that this new antibody selectively recognizes the antiparallel topology of the telomeric G4 sequence, a property further validated in cellular models.

biochemistry↗

bioRxiv2025

Mechanical forces drive mitochondrial matrix extrusion and apoptotic pore growth

Apoptotic pore opening by BAX and BAK at the mitochondrial outer membrane is a key step in the cell commitment to death. The subsequent inner membrane extrusion and permeabilization releases mitochondrial DNA into the cytosol, which can trigger inflammatory signaling. However, the underlying mechanisms have not been elucidated. Here we developed CLOSE microscopy, a multi-correlative approach that enabled the simultaneous analysis of BAK stoichiometry and nanoscale organization in individual apoptotic pore complexes in relation to mitochondrial ultrastructure. We find that the outer membrane opening at the apoptotic pore defines the spatial arrangement of BAK nanoassemblies. We identify mechanical stress as a driver of inner membrane extrusion, which can be perturbed by osmoregulation. The extruded inner membrane in turn exerts forces on the outer membrane that promote apoptotic pore growth, in line with membrane dynamics simulations. Our study reveals a tight interplay between the inner and outer membranes during mitochondrial permeabilization in apoptosis and establishes a biophysical mechanism for inner membrane extrusion that defines the structural organization of the apoptotic pore.

cell biology↗

bioRxiv2024

Identifying the Fusarium species involved in foot rot disease of faba beans in the UK using a combined molecular and microbiological approach

Foot rot is a devastating disease of faba bean crops globally, including in the United Kingdom, the worlds third largest producer. To identify the causal agents, we have sampled foot rot-affected plants and soils from faba bean crops across England. We isolated organisms associated with foot rot disease in culture and assessed pathogenicity in vivo to evaluate the infectivity of the isolates on faba bean. We identified the pathogenic isolates using DNA barcoding of the Internal Transcribed Spacer (ITS) and Translation Elongation Factor one (TEF1 ) molecular markers. A total of 113 clonal isolates were obtained from infected plants and soil samples across England. Of these, 60 were pathogenic, inducing mild to severe symptoms on faba bean. Sequencing of the ITS and TEF1 loci and comparison against sequence databases (Genbank and Fusarium_ID) enabled the identification of pathogenic isolates, in decreasing order of frequency, as Fusarium oxysporum (26.6 %), F. vanettenii (25%), F. redolens (15 %), F. solani (11.6%), F. culmorum (8.3 %), F. avenaceum (6.7 %), F. equiseti (1.7 %), F. clavum (1.7 %), Clonostachys rosea (1.7%) and Alternaria alternata (1.7%). F. oxysporum, F. redolens and F. avenaceum induced the most severe symptoms, whilst F. solani induced the least severe symptoms. Determining the most prevalent causal agents of foot rot in UK faba beans will facilitate targeted disease monitoring and intervention for enhanced productivity.

microbiology↗

bioRxiv2023

iMab Antibody Binds Single-Stranded Cytosine-Rich Sequences and Unfolds DNA i-Motifs

i-Motifs (iMs) are non-canonical, four-stranded secondary structures formed by stacking of hemi-protonated CH+{middle dot}C base pairs in cytosine-rich DNA sequences, predominantly at pH < 7. The presence of iM structures in cells was a matter of debate until the recent development of iM-specific antibody, iMab, that was instrumental for several studies that suggested the existence of iMs in live cells and their putative biological roles. We assessed the interaction of iMab with cytosine-rich oligonucleotides by biolayer interferometry (BLI), pull-down assay and bulk-FRET experiments. Our results suggest that binding of iMab to DNA oligonucleotides is governed by the presence of runs of at least two consecutive cytosines and is generally increased in acidic conditions, irrespectively of the capacity of the sequence to adopt, or not, an iM structure. Moreover, the results of the bulk-FRET assay indicate that interaction with iMab results in unfolding of iM structures even in acidic conditions (pH 5.8 or 6.5), similarly to what has been observed with hnRNP K, well-studied single- stranded DNA binding protein. Taken together, our results suggest that iMab actually binds to blocks of 2-3 cytosines in single-stranded DNA, and call for more careful interpretation of results obtained with this antibody.

biophysics↗

bioRxiv2023

Large-scale phenotypic and genomic characterization of Listeria monocytogenes susceptibility to quaternary ammonium compounds

Listeria monocytogenes is a significant concern for the food industry due to its ability to persist in the food processing environment. Decreased susceptibility to disinfectants is one of the factors that contribute to the persistence of L. monocytogenes. The objective of this study was to explore the diversity of L. monocytogenes susceptibility to quaternary ammonium compounds (QACs) using 1,671 L. monocytogenes isolates. This was used to determine the phenotype-genotype concordance and characterize genomes of the QAC sensitive and tolerant isolates for stress resistance, virulence and plasmid replicon genes. Distribution of QAC tolerance genes among 37,897 publicly available L. monocytogenes genomes were also examined. The minimum inhibitory concentration to QACs was determined by the broth microdilution method and non-sequenced isolates (n=1,244) were whole genome sequenced. Genotype-phenotype concordance was 99% for benzalkonium chloride, DDAC and a commercial QAC based sanitizer. Prevalence of QAC tolerance genes was 23% and 28% in our L. monocytogenes collection and in the global dataset, respectively. qacH was the most prevalent gene in our collection (61%), with 19% prevalence in the global dataset. Notably, bcrABC was most common (72%) globally, while 25% in our collection. Prevalence of emrC and emrE was comparable in both datasets, 7% and 2%, respectively. Replicon genes, indicative of plasmid harborage, were detected in 44% of the isolates and associated with the QAC tolerant phenotype. The presented analysis is based on the biggest L. monocytogenes collection in diversity and quantity for characterization of the L. monocytogenes QAC tolerance at both phenotypic and genomic levels. IMPORTANCEContamination of Listeria monocytogenes within the food processing environment is of concern to the food industry due to challenges in eradicating the pathogen once it becomes persistent in the environment. Genetic markers associated with increased tolerance to disinfectants have been identified, which alongside factors favor the persistence of L. monocytogenes in the production environment. By employing a comprehensive large-scale phenotypic testing and genomic analysis our study significantly enhances the understanding of the prevalence of quaternary ammonium compound (QAC) tolerant L. monocytogenes and the genetic determinants associated with the increased tolerance. Furthermore, we report on the prevalence of QAC tolerance genes among 37,897 publicly available L. monocytogenes sequences and their distribution within clonal complexes, isolation sources and geographical locations. As the propagation of QAC tolerance showed not be evenly distributed globally this highlights that understanding the development of L. monocytogenes disinfectant tolerance can be monitored using publicly available WGS data.

microbiology↗

bioRxiv2023

KAT6A mutations in Arboleda-Tham syndrome drive epigenetic regulation of posterior HOXC cluster

Arboleda-Tham Syndrome (ARTHS) is a rare genetic disorder caused by heterozygous, de novo truncating mutations in Lysine(K) acetyltransferase 6A (KAT6A). ARTHS is clinically heterogeneous and characterized by several common features including intellectual disability, developmental and speech delay, hypotonia and affects multiple organ systems. KAT6A is highly expressed in early development and plays a key role in cell-type specific differentiation. KAT6A is the enzymatic core of a histone-acetylation protein complex, however the direct histone targets and gene regulatory effects remain unknown. In this study, we use ARTHS patient (n=8) and control (n=14) dermal fibroblasts and perform comprehensive profiling of the epigenome and transcriptome caused by KAT6A mutations. We identified differential chromatin accessibility within the promoter or gene body of 23%(14/60) of genes that were differentially expressed between ARTHS and controls. Within fibroblasts, we show a distinct set of genes from the posterior HOXC gene cluster (HOXC10, HOXC11, HOXC-AS3, HOXC-AS2, HOTAIR) that are overexpressed in ARTHS and are transcription factors critical for early development body segment patterning. The genomic loci harboring HOXC genes are epigenetically regulated with increased chromatin accessibility, high levels of H3K23ac, and increased gene-body DNA methylation compared to controls, all of which are consistent with transcriptomic overexpression. Finally, we used unbiased proteomic mass spectrometry and identified two new histone post-translational modifications (PTMs) that are disrupted in ARTHS: H2A and H3K56 acetylation. Our multi-omics assays have identified novel histone and gene regulatory roles of KAT6A in a large group of ARTHS patients harboring diverse pathogenic mutations. This work provides insight into the role of KAT6A on the epigenomic regulation in somatic cell types.

genomics↗

bioRxiv2023

Clearwing butterflies challenge the thermal melanism hypothesis

In contrast to most butterflies harboring opaque wing colorations, some species display large transparent patches on their wings. Wing transparency, which entails a dramatic reduction of pigmentation, raises the question of potential costs for vital functions, such as thermoregulation, especially along climatic gradients. The thermal melanism hypothesis posits that darker colorations should be favored in colder environments, which enables them to absorb more radiation and maintain a body temperature compatible with activity. This prediction extends to the near infrared (NIR) range, which represents a large proportion of solar radiation. Here we assess the implications of wing transparency for light absorption and thermal properties in 42 butterfly species from the neotropical tribe Ithomiini that range the extent of transparency, from fully opaque to highly transparent, and we test whether those species conform to the prediction of the thermal melanism hypothesis. We find that transparent wings are less efficient than opaque wings to absorb light across UV, Visible and NIR wavelength ranges, and are also less efficient to collect heat. Moreover, dark coloration occupies a lower proportion of wing area as altitude increases, and ithomiine species harbor more transparency at higher altitudes, where climatic conditions are colder, going strongly against the prediction of the thermal melanism hypothesis. We discuss these surprising results in light of recent studies suggesting that factors other than adaptation to cold, such as predation pressure, physiology or behavior, may have driven the evolution of wing patterns in Ithomiini. Significance StatementThe thermal melanism hypothesis predicts that organisms should be darker and absorb solar radiation more efficiently in colder environments. The Neotropical butterflies Ithomiini are unusual in that many species harbor large transparent patches on their wings, raising questions related to their efficacy of solar radiation absorption and heating capacities. We investigate optical and thermal properties of several ithomiine species along a climatic gradient. We find that transparent wings are less efficient at absorbing radiation and collecting heat. Unexpectedly, the proportion of transparent species increases with altitude, challenging the thermal melanism hypothesis and suggesting that factors other than adaptation to cold, such as predation pressure, may have driven the evolution of wing patterns in Ithomiini.

evolutionary biology↗

bioRxiv2022

Functional traits trade-offs define plant population stability worldwide

O_LIEcological theory posits that temporal stability patterns in plant populations are associated with differences in species ecological strategies. However, empirical evidence is lacking about which traits, or trade-offs, underlie species stability, specially across different ecosystems. C_LIO_LITo address this, we compiled a global collection of long-term permanent vegetation records (>7000 plots from 78 datasets) from a wide range of habitats and combined this with existing trait databases. We tested whether the observed inter-annual variability in species abundance (coefficient of variation) was related to multiple individual traits and multivariate axes of trait variations (PCoA axes). C_LIO_LIWe found that species with greater leaf dry matter content and seed mass were consistently more stable over time (lower variability in species abundance) although other leaf traits played a significant role as well, albeit weaker. Using multivariate axes did not improve predictions by specific traits. C_LIO_LIOur results confirm existing theory, providing compelling empirical evidence on the importance of specific traits, which point at ecological trade-offs in different resource use and dispersal strategies, on the stability of plant populations worldwide. C_LI

ecology↗

bioRxiv2021

Hydrophobicity in clearwing butterflies and moths: impact of scale 2 micro and nanostructure, and trade-off with optical transparency

Living organisms are submitted to multiple developmental and selective constraints resulting in evolutionary compromises, one of the best examples being the integument (the outer protective layer of living organisms) which is fundamentally multifunctional. Integument anti-wetting or hydrophobicity - evolved in relation to complex and various structures - is a crucial property as it serves multiple functions like self-cleaning, locomotion, or defence against pathogens and may interfere with other functions like thermoregulation or communication. Elucidating the structure-property relationships and unravelling potential trade-offs is crucial to understand the evolution of the integument. In opaque Lepidoptera, wing scales actively contribute to anti-wetting. In clearwing Lepidoptera, wing scales are often reduced, raising the question of whether they can maintain similar hydrophobicity levels to those of opaque species and if not, whether wing microstructure (scale density, shape, insertion, and coloration) may mitigate the costs of a lower hydrophobicity. To answer these questions, we measure static contact angle (CA) of water droplets at different stages of evaporation in opaque and transparent patches of 23 Lepidoptera species that show a high diversity in wing microstructure. More specifically, we find that transparency is costly for hydrophobicity, and that such cost depends on wing microstructure. In general, transparent patches lose more hydrophobicity with water evaporation than opaque patches. Yet, this loss of hydrophobicity is attenuated for higher scale densities, erect scales compared to flat scales, coloured scales (for erect scales), multiple scale layers (for flat scales), or when combining two types of scales (piliform and lamellar) than having only one type of scale (piliform or lamellar). Nude membranes show the lowest hydrophobicity values. We find that wing hydrophobicity negatively relates to optical transparency, showing a trade-off between optics and hydrophobicity. Moreover, we find that tropical species have higher hydrophobicity in their transparent patches than temperate ones, suggesting transparent patches are under stronger selection for hydrophobicity in tropical than in temperate species. These novel findings, which are consistent with the physics of hydrophobicity, suggest that insect wings are evolutionary multifunctional compromises.

evolutionary biology↗