Biology subjects

Garcia, G.

Publications and source records attributed to Garcia, G..

At least 19 recordsLinked to original sources

bioRxiv2026

Expression of tardigrade intrinsically disordered proteins in C. elegans reveals variable effects on aging and stress

Tardigrades survive extreme environmental stress by expressing intrinsically disordered proteins that stabilize cellular structures during cryptobiosis. Because these proteins protect cells from desiccation, oxidative stress, and DNA damage, they have attracted interest as potential therapeutics to enhance stress resilience in other organisms. However, most studies have relied on cultured cells or germline expression, leaving their effects in somatic tissues largely unexplored. Here, we generated Caenorhabditis elegans strains expressing four tardigrade intrinsically disordered proteins, Damage Suppressor (DSUP), cytoplasmic-abundant heat-soluble (CAHS), mitochondrial-abundant heat-soluble (MAHS), and Ramazzottius varieornatus late embryogenesis abundant (RvLEAM), throughout somatic tissues. Surprisingly, constitutive expression of each protein reduced lifespan, impaired motility and reproduction, and failed to improve resistance to most environmental stressors. DSUP toxicity was tissue- and developmental stage-dependent, indicating that both spatial and temporal expression influence its physiological effects. Despite these detrimental phenotypes, several proteins reduced protein aggregation during desiccation-associated stress, demonstrating context-dependent protective effects. Together, our findings reveal that tardigrade stress proteins impose physiological tradeoffs in vivo and underscore the importance of evaluating candidate stress-protective proteins in physiologically relevant somatic models before therapeutic translation.

genetics↗

bioRxiv2026

The constitutive androstane receptor protects against metabolic dysfunction-associated steatotic liver disease through sex specific interactions with the gut microbiota

Background: The gut-liver axis is involved in Metabolic dysfunction-Associated Steatotic Liver Disease (MASLD), but the host molecular actors involved in such dialogue have not yet been fully characterized. Objective: We investigated the sex-dependent role of the Constitutive Androstane Receptor (CAR) as a hepatic sensor of microbial signals in MASLD pathophysiology. Design: Male and female Car+/+ and Car-/- mice were fed a western diet (WD) for 4, 14 or 35 weeks. We performed plasma biochemistry, liver histology, bile acid and cholesterol quantification, untargeted multi-omics approach combining liver RNA-sequencing and 16S rRNA sequencing, together with co-housing, fecal microbiota transplantation and analysis of publicly available transcriptomics data in human cohorts. Results: Short-term WD revealed CAR-dependent protection against steatosis, together with perturbations in the transcriptional signatures of multiple transcription factors involved in hepatocyte identity in males. After 14 weeks, CAR deletion increased WD-induced liver damage, inflammation and fibrosis, and disrupted bile acid, cholesterol and gut microbiota homeostasis, in males only. Co-housing and fecal microbiota transplantations revealed that a Car+/+ gut microbiota protected against WD-induced liver damage, while a Car-/- microbiota was reshaped by a Car+/+ host. No CAR-dependent phenotype was observed in females. Finally, in human cohorts, hepatic CAR expression decreased in advanced clinical stages of MASLD. Conclusion: CAR is a sex-dependent protective nuclear receptor against MASLD progression, acting both as a transcriptional regulator of hepatocyte identity and as a mediator of the host-microbiota crosstalk.

physiology↗

bioRxiv2026

PPARα-dependent effects in the liver and jejunum of mice in response to pemafibrate

Peroxisome proliferator-activated receptor (PPAR) is a nuclear receptor that plays a central role in metabolic adaptation by regulating gene expression programs involved in lipid utilization and energy homeostasis. Although the hepatic functions of PPAR and its target genes are well characterized, less is known about its transcriptional activity in extrahepatic tissues. Pemafibrate (K-877), a selective PPAR modulator (SPPARM), is a high-affinity PPAR ligand with improved potency and selectivity compared with conventional fibrates. Here, we investigated pemafibrate-induced tissue-specific transcriptional responses comparing wild type and whole-body PPAR-deficient littermate mice. Twelve-week-old male PPAR+/+ and PPAR-/- mice were treated daily with pemafibrate (0.1 mg/kg) or vehicle by oral gavage for 14 days. We performed genome-wide transcriptomic analyses in the liver, jejunum, kidney, soleus muscle, and BAT. Pemafibrate-induced transcriptional changes were entirely dependent on PPAR, as no differentially expressed genes were detected in PPAR-/- mice. The magnitude and nature of the response were tissue-specific, with the strongest transcriptional effects observed in the liver and jejunum, whereas the kidney, soleus muscle, and BAT showed limited responses. In the liver, pemafibrate primarily induced the expression of genes involved in fatty acid metabolism, mitochondrial function, and energy production. In the jejunum, pemafibrate activated lipid metabolic programs together with tissue-specific pathways related to cellular homeostasis. Collectively, our findings show that pemafibrate is a highly selective PPAR activator with a preferential transcriptional activity in the liver and intestine after oral administration. This study provides a resource for defining tissue-specific PPAR-responsive gene networks and expands our understanding of PPAR functions beyond the liver.

pharmacology and toxicology↗

bioRxiv2026

Multi-omics Reveals Divergent Endothelial Molecular Responses to New and Old World Hantaviruses

Hantaviruses cause vascular leakage syndromes that vary in clinical manifestation and severity. Although tissue tropism contributes to these differences, both Old and New World hantaviruses infect endothelial cells, where species-specific disease phenotypes remain poorly understood. Here we integrated time-resolved global RNA sequencing, mass spectrometry proteomics, and phosphoproteomics of human endothelial cells infected with New World Andes virus (ANDV) or Old World Hantaan virus (HTNV). Despite equivalent early viral RNA and protein levels, ANDV elicited a stronger innate immune protein response, preceding its restriction while HTNV replication continued. At later stages of infection, HTNV induced downregulation of cytoskeletal and junctional protein phosphorylation, accompanied by visual disruption of cellular actin architecture. Additionally, ANDV induced heightened activity of ERBB-family kinases, whose chemical inhibition by neratinib and afatinib reduced viral replication. Together, these data define species-specific responses in endothelial cells, identify druggable host targets, and reveal mechanisms with relevance to divergent vascular leakage symptomology.

systems biology↗

bioRxiv2026

Conserved covariance structure underlies 60 million years of morphological diversification in primates

Evolvability, the capacity of populations to respond to selection, is shaped by the structure and amount of variation transmitted from generation to generation. Whether the heritable covariance structure itself remains stable or evolves rapidly is a central, yet unresolved, question in phenotypic evolution. Competing hypotheses suggest that trait covariation may be constrained by developmental and genetic architectures or, alternatively, reshaped by persistent directional selection. Here, we test whether covariance structure and evolvability are stable over macroevolutionary timescales by applying a comparative evolutionary quantitative genetics framework on primates. We quantified cranial variation using over ten thousand specimens representing 309 species and compared phenotypic covariance matrices for 57 genera within a Bayesian framework. Our results show that despite extensive morphological divergence, primates show remarkably conserved patterns of variation, modular organization, and capacity to respond to selection. Reconstruction of selection gradients across the primate radiation revealed that selection was highly structured, with preferential directions aligned with major axes of cranial variation. These results suggest that the stability of evolvability does not reflect evolutionary stasis, but rather emerges from the alignment between conserved developmental architecture and selection. Our findings demonstrate that covariance structure and the evolutionary potential it provides can persist over deep evolutionary timescales, providing a mechanistic framework for understanding how developmental systems shape the trajectories of major radiations.

evolutionary biology↗

bioRxiv2026

Candidozyma auris utilizes transferrin, but not heme-bound iron for in vivo virulence

Candidozyma auris (C. auris) is an emerging multidrug-resistant fungal pathogen, and its dissemination to the bloodstream and deep-seated organs is associated with high mortality. The limited antifungal armory and pipelines against C. auris pose a major challenge in disease management. Addressing this threat requires a deeper understanding of fungal virulence mechanisms that promote persistence and of host factors that drive susceptibility. Previous in vitro studies showed that iron enhances C. auris resistance to azoles and echinocandins, whereas iron chelation mitigates this effect. Here, we demonstrate that C. auris does not utilize cell-free heme or induce hemolysis but instead extracts and uses iron from transferrin to support growth and virulence. Deletion of the SIT1 siderophore transporter in C. auris attenuated fungal growth and reduced renal injury, while increased transferrin-iron saturation worsened disease outcomes in immunocompetent mice, highlighting the importance of transferrin-bound iron uptake. Mechanistically, C. auris exploits transferrin-bound iron to enhance ergosterol biosynthesis and activate antioxidant defenses, promoting resistance to neutrophil- and caspofungin-mediated killing. These findings identify elevated transferrin saturation as a novel host susceptibility risk factor for disseminated C. auris infection and reveal how iron availability reshapes fungal physiology to drive infection persistence.

microbiology↗

bioRxiv2026

Revealing the spatiotemporal dynamics of methionine metabolism with a genetically encoded single-fluorophore biosensor

Methionine is an essential amino acid, used for protein synthesis, redox homeostasis, and methylation reactions throughout the cell. However, the compartmentalized dynamics of methionine have remained elusive, due to a lack of available tools to measure methionine with high spatial and temporal resolution. To address this limitation, we have developed a single fluorescent protein-based methionine optical reporter (Meteor) which reports subcellular changes in methionine with high dynamic range. Using Meteor, we demonstrate the subcellular uptake of methionine in multiple cell lines into several locations, including the mitochondrial matrix. Furthermore, we use Meteor to illuminate the dynamics of the methionine cycle in the cytoplasm and nucleus, finding cancer cells can rapidly increase methionine from metabolic precursors in both locations. Finally, demonstrated that Meteor can be used to visualize methionine dynamics in vivo using Caenorhabditis elegans. Thus, we have developed a new tool to measure methionine dynamics across scales with high dynamic range and spatiotemporal resolution.

biochemistry↗

bioRxiv2026

HIRA-mediated H3.3 deposition preserves hepatocyte cell identity during liver aging

Age-associated functional decline is partly driven by progressive chromatin degeneration. Maintenance of chromatin integrity preserves cell identity and promotes healthy aging, but through different mechanisms in proliferating and non-proliferating cells. However, specific mechanisms of chromatin maintenance and their compensatory capacity in proliferating and non-proliferating cells are undefined. The histone chaperone HIRA deposits the histone variant H3.3 in a DNA replication-independent manner, leading to its accumulation in aging, non-proliferating cells. Here, we show that hepatocyte-specific loss of HIRA causes loss of cell identity, metabolic dysfunction, and accelerated fibrotic pathology with age. Transcriptomic and epigenomic analyses indicate that HIRA-H3.3 preserves chromatin integrity and sustains transcription of highly expressed genes, including cell identity genes. Partial hepatectomy, associated with induced proliferation, restores identity of HIRA knockout livers with compensatory deposition of canonical histones H3.1/2. Together, these results demonstrate that HIRA-mediated H3.3 deposition is essential for safeguarding cell identity and tissue function during aging of non-proliferating cells, but this function can be rescued by tissue regeneration and associated cell proliferation. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=124 SRC="FIGDIR/small/710643v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@a2a26aorg.highwire.dtl.DTLVardef@154e5aeorg.highwire.dtl.DTLVardef@b315a7org.highwire.dtl.DTLVardef@152bca4_HPS_FORMAT_FIGEXP M_FIG C_FIG

genomics↗

bioRxiv2026

A non-canonical role for UPRER during heat stress in C. elegans.

Organisms rely on coordinated stress responses to maintain cellular homeostasis. Perhaps the best-known example of multiple stress inputs converging onto a single response is the integrated stress response (ISR), which reduces global translation under various stress conditions to reduce the protein folding burden of the cell. Similarly, most stress responses generally involve coordination of additional protein homeostasis (proteostasis) pathways, including increased expression of chaperones to refold proteins, as well as activation of clearance mechanisms, such as autophagy and the ubiquitin proteosome system. Our study investigates how heat stress can influence coordinated activation of both cytosolic and ER chaperones, exploring bidirectional cross talk between canonical activators of the cytosolic heat-shock response (HSR) and the unfolded protein response of the ER (UPRER). Using robust transcriptional reporters in the C. elegans model system, we explore a non-canonical activation of the UPRER under heat stress by the coordinated effects of XBP-1 and HSF-1. We further investigate inter tissue communications of stress whereby neuronal or glial activation of the UPRER can result in heterotypic enhancement of the HSR in peripheral and can increase thermotolerance. This work highlights the complex convergence of cellular stress responses, a phenomenon that may reflect a general strategy wherein localized stress can activate numerous proteostasis pathways to prevent whole cell and whole organism damage. Article SummaryA reductionist approach to studying cellular stress responses is critical for dissecting specific molecular and genetic drivers of stress response. However, stress responses are often convergent and overlapping, and these single input and output studies may miss their complex interplay. Many studies have revealed the intricate coordination of stress responses, including the ability of seemingly organelle-specific stress responses, like mitochondrial stress responses, to directly influence cytosolic and ER health. Our study adds to this growing field by describing a unique, bidirectional crosstalk between the cytosolic and ER stress pathways, highlighting systemic coordination of stress resilience.

genetics↗

bioRxiv2025

Cryo-ET Reveals Distinct Gag Lattice Architectures in Virus-like Particles and Immature HIV-1

HIV-1 is released from infected cells as immature virions whose membranes are supported by a Gag lattice. During maturation, this lattice is cleaved by the viral protease to release capsid proteins that assemble into the mature core. The architecture of the Gag lattice is central to this process, and the Gag lattice is targeted by maturation inhibitors that block cleavage. Using cryo-electron tomography, we compared Gag-only virus-like particles (VLPs) with immature HIV-1 virions and found that VLPs assemble denser and more complete lattices, exhibiting a strong correlation between lattice curvature and Gag copy number. In contrast, immature virions incorporate fewer Gag molecules and display weaker coupling between curvature and Gag stoichiometry. These findings show that while Gag alone can form the canonical immature lattice, additional viral components fine-tune lattice organization and curvature, potentially regulating protease accessibility, virion release, and the onset of HIV-1 maturation.

biophysics↗

bioRxiv2025

Form and function of actin impacts actin health and aging.

The actin cytoskeleton is a fundamental and highly conserved structure that functions in diverse cellular processes, yet its direct contribution to organismal aging remains unclear. Here, we systematically interrogated how genetic and pharmacologic perturbations of actin structure and function influence lifespan and various hallmarks of aging in Caenorhabditis elegans. Whole-animal and tissue-specific knockdown of actin and key actin-binding proteins (ABPs) - arx-2 (Arp2/3), unc-60 (cofilin), and lev-11 (tropomyosin) - led to premature disruption of filament organization, reduced lifespan, and tissue-specific physiological defects. Bulk and single-nucleus RNA-sequencing revealed that ABP knockdowns elicited a strongly "aged" transcriptome. Actin dysfunction broadly exacerbated many age-associated phenotypes, including mitochondrial dysfunction, lipid dysregulation, loss of proteostasis, impaired autophagy, and intestinal barrier failure. Pharmacological destabilization with Latrunculin A mirrored genetic knockdowns, while mild stabilization with Jasplakinolide modestly extended lifespan, emphasizing that optimal and finely-tuned actin function is critical for healthy aging. Finally, analysis of human genome-wide association data revealed that common ACTB polymorphisms correlate with differences in age-related decline in gait speed, suggesting evolutionary conservation of actins role in healthy aging. Taken together, our results provide a comprehensive and publicly accessible resource that maps, for the first time, how actin integrity intersects with diverse aging pathways across tissues and scales. This descriptive framework is intended to enable future mechanistic discovery by offering a deep, unbiased dataset that can be integrated with emerging studies to define how actin dynamics contribute to aging.

cell biology↗

bioRxiv2025

Efficient genetic perturbation of murine sensory neurons in vivo using CRISPR/Cas9

Gene editing using CRISPR/Cas9 in vivo offers a powerful tool to investigate pain mechanisms. We validated the use of conditional knock-in mouse model expressing Streptococcus pyogenes CRISPR associated protein 9 selectively in sensory neurons by crossing with Scn10a-Cre driver. Transgene expression was confirmed in key tissues including the dorsal root ganglia (DRG) and sciatic nerve. To assess in vivo editing efficacy, RNA guides targeting GFP or TRPV1 were intrathecally administered. A dose of 3 {micro}g RNA guides significantly reduced GFP expression, and two rounds of nanoparticle delivery targeting TRPV1 resulted in [~]65% reduction in DRG and [~]55% in sciatic nerve without triggering caspase-3-mediated apoptosis or motor deficits. Edited animals exhibited increased withdrawal latencies to heat and reduced nocifensive behaviors following capsaicin injection. Their responses to capsaicin-evoked thermal hyperalgesia and mechanical allodynia were diminished. This approach enables rapid and efficient sensory neuron-specific CRISPR/Cas9 gene perturbations for pain research in mice. We envisage that this method can be employed both for the exploration of molecular mechanisms underlying nociception and for the validation of therapeutic targets associated with pain.

neuroscience↗

bioRxiv2025

Genome Report: De novo genome assembly of the greater Bermuda land snail, Poecilozonites bermudensis (Mollusca:Gastropoda), confirms ancestral genome duplication

Poecilozonites bermudensis, the greater Bermuda land snail, is a critically endangered species and one of only two extant members in its genus. These snails are one of Bermudas few endemic animal clades and their rich fossil record was the basis for the punctuated equilibria model of speciation. Once thought extinct, recent conservation efforts have focused on the recovery of the species, yet no genomic information or other molecular sequences have been available to inform these initiatives. We present a high-quality, annotated genome for P. bermudensis generated using PacBio long read and Omni-C short read sequencing. The resulting assembly is approximately 1.36 Gb with a scaffold N50 of 44.t Mb and 31 chromosome-length scaffolds. Nearly 43 percent of the genome was identified as repeat content. This assembly will serve as a resource for the conservation and study of P. bermudensis, and its only close extant and also critically endangered relative, P. circumfirmatus. Additionally, this genome adds to the growing body of data needed for a more complete understanding of gastropod evolution and for evolutionary processes in general. Article summaryThis paper is aimed primarily at researchers studying genomic evolution and phylogenetics of mollusks, and secondarily researchers studying evolution and conservation of Bermuda land snails. It reports not only the first genome sequence for the Bermuda land snails, but the first sequence of any kind from the group and the first genome from the larger clade to which they belong. The paper presents a complete de novo genome annotation and first order analyses. The results support previous hypotheses that a genome duplication occurred at the base of land snails, and they facilitate future molecular work on Bermudian and other snails.

genomics↗

bioRxiv2025

Dual-feature selectivity enables bidirectional coding in visual cortical neurons

Sensory neurons are traditionally viewed as feature detectors that respond with an increase in firing rate to preferred stimuli while remaining unresponsive to others. Here, we identify a dual-feature encoding strategy in macaque visual cortex, wherein many neurons in areas V1 and V4 are selectively tuned to two distinct visual features--one that enhances and one that suppresses activity--around an elevated baseline firing rate. By combining neuronal recordings with functional digital twin models--deep learning-based predictive models of biological neurons--we were able to systematically identify each neurons preferred and non-preferred features. These feature pairs served as anchors for a continuous, low-dimensional axis in natural image similarity space, along which neuronal activity varied approximately linearly. Within a single visual area, visual features that strongly or weakly activated individual neurons also had a high probability of modulating the activity of other neurons, suggesting a shared feature selectivity across the population that structures stimulus encoding. We show that this encoding strategy is conserved across species, present in both primary and lateral visual areas of mouse cortex. Dual-feature selectivity is consistent with recent anatomical evidence for feature-specific inhibitory connectivity, complementing the feature-detector principle through circuit mechanisms in which selective excitation and inhibition may together enhance the representational capacity of the neuronal population.

neuroscience↗

bioRxiv2025

Drug screen reveals new potent host-targeted antivirals against Mpox virus

Mpox virus (MPXV), a re-emerging zoonotic threat, has caused outbreaks in non-endemic regions through respiratory, sexual, and close-contact transmission. The increased transmissibility of Clade IIb fueled the 2022 global outbreak, with 2024 Clade Ib spread in the Democratic Republic of Congo further escalating concern. Both outbreaks were declared public health emergencies by the WHO. Although tecovirimat (TPOXX) has been used off-label for Mpox, its limited effectiveness highlights the critical need for newer antivirals for MPXV. We conducted high- throughput antiviral drug screening using a host-directed kinase inhibitor library composed of 2,750 compounds against 2022 Clade IIb MPXV. Our primary screen identified 138 compounds preventing MPXV cytopathic effects, including multiple inhibitors of EGFR, PI3K-mTOR, and Ras/Raf, as well as apoptosis and autophagy regulators. Secondary and tertiary screenings yielded a shortlist of potent, nontoxic antiviral compounds that inhibited MPXV replication. Three selected compounds, IRAK4-IN-6, SM-7368, and KRAS inhibitor-10, reduced MPXV-induced cell death in primary human epidermal keratinocytes. IRAK4-IN-6 and SM-7368 were also found to modulate NF-{kappa}B and STING signaling. Furthermore, these compounds were found effective in reducing skin lesions and viral burden in a mouse model of MPXV skin infection. Together, our study reveals new classes of antiviral compounds against MPXV, offering promising candidates for future clinical development.

microbiology↗

bioRxiv2025

Transcriptomic analysis of mitohormesis associated with lifespan extension in Caenorhabditis elegans

Non-lethal exposure to mitochondrial stress has been shown to have beneficial effects due to activation of signalling pathways, including the mitochondrial unfolded protein response (UPRmt). Activation of UPRmt restores function of the mitochondria and improves general health and longevity in multiple model systems, termed mitohormesis. In C. elegans, mitohormesis can be accomplished by electron transport chain inhibition, decline in mitochondrial translation, decreased mitochondrial import, and numerous other methods that activate UPRmt. However, not all methods that activate UPRmt can promote longevity. These and other studies have started to question whether UPRMT is directly correlated with longevity. Here, we attempt to address this controversy by unravelling the complex molecular regulation of longevity of the nematode under different mitochondrial stressors that induce UPRmt by performing RNA-sequencing to profile transcriptome changes. Using this comprehensive and unbiased approach, we aim to determine whether specific transcriptomic changes can reveal a correlation between UPRmt and longevity. Altogether this study will provide mechanistic insights on mitohormesis and how it correlates with lifespan of C. elegans.

systems biology↗

bioRxiv2025

A systematic review of climate-change driven range shifts in mosquito vectors

As global temperatures rise, concerns about shifting mosquito ranges--and accompanying changes in the transmission of malaria, dengue, and other diseases--are mounting. However, systematic evidence for climate-driven changes in mosquito ranges remains limited. We conducted a systematic review of studies documenting expansions or contractions in medically important mosquito species. In total, 178 studies on six continents identified range expansions in 118 mosquito species. While over a third of these studies cited warming as a driver, fewer than 10% performed statistical tests of the role of climate. Instead, most expansions were linked to human-aided dispersal (e.g., trade, travel), land-use changes, and urbanization. Although several studies reported poleward or upward expansions consistent with climate warming, none demonstrated warm-edge contractions driven by rising temperatures, which are theoretically predicted in some settings. Rather than expanding into newly suitable areas, many expansions appear to be filling preexisting thermally suitable habitats. Our findings highlight the need for long-term mosquito monitoring, rigorous climate-attribution methods, and better documentation of confounding factors like land-use change and vector control efforts to disentangle climate-driven changes from other anthropogenic factors.

ecology↗

bioRxiv2025

Mosquito Dispersal in Context

Mosquito dispersal plays an important role in mosquito ecology and mosquito-borne pathogen transmission. While reaction-diffusion and patch-based models with simple flux assumptions for emigration have played a predominant role in modeling mosquito dispersal, mosquito behavioral ecology - in particular, the process of searching for resources - is usually ignored by diffusion-based models. We thus set out to analyze mosquito movement using highly mimetic models, to see what we could learn from a different approach. Here, we present two behavioral state microsimulation models, in which mosquitoes are in behavioral states and search for required resources, which are distributed on a landscape. Models of this sort are laborious and challenging to work with, so we developed ramp.micro, an R package to build, solve, analyze, and visualize behavioral state microsimulation models for mosquitoes. Mosquito population dispersal is an emergent feature in these complex systems, so we developed new methods to describe and understand it. We show that population structure might not be revealed by a crude analysis of observed mosquito movement patterns, unless it can somehow account for sequences of flights for mosquitoes in behavioral states trying to accomplish a goal. We also show that even when resources are distributed randomly and uniformly, mosquito populations tend to form highly spatially structured communities. We also show that some heterogeneity in mosquito population densities is attributed to features of a network defined by searching and the spatial distribution of resources. These models highlight the importance of understanding mosquito behavioral states and resource availability in understanding mosquito population dispersal, and they point to the importance of local context. Motivated by these dynamics, spatial models for mosquito ecology and mosquito-borne pathogen transmission would benefit from considering resource availability as a factor affecting mosquito movement and dispersal. Author summaryWe develop highly realistic population dynamic models for mosquito behavioral ecology where mosquitoes move around on landscapes made up of resources located at points in space. The mosquitoes are in behavioral states - blood feeding, egg laying, or sugar feeding - and they end each search at a point where the resource they need can be found. Even with simple assumptions, mosquito populations can be highly structured. Because mosquitoes tend to leave areas that lack a resource, and they tend to stay in areas that have all required resources, the scarcest resources end up determining the structure of mosquito populations.

ecology↗