PLOS Biology

Triatominae bugs are the main vectors of Chagas disease in Latin America and rely on microbial nutritional symbiosis to complement their haematophagous diet with B-vitamins. While Rhodococcus bacteria have been identified as key symbionts, diverse metabarcoding analyses have suggested additional candidates. However, symbiont genomic data and metabolic capabilities remain largely uncharacterized. To address this gap, we generated metagenomic assemblies for 14 Triatominae and captured 15 bacterial genomes belonging to 4 genera (Rhodococcus, Wolbachia, Symbiopectobacterium and Arsenophonus) across 9 triatominae species. We identified five co-infection cases, including one involving two distinct Arsenophonus symbionts, one exhibiting hallmarks of massive genome degradation. Phylogenetic analyses revealed that Triatominae-associated symbionts form monophyletic groups within each genus, suggesting common origins followed by co-evolution with their hosts. Annotation of vitamin B metabolic genes indicates that most symbionts harbour incomplete pathways, with evidence of metabolic complementation between co-infecting symbionts. Additionally, we identified bacterial genes laterally transferred into host insect genomes, interpreted as footprints of present or past symbiotic associations. Nearly all Triatominae genomes displayed transferred genes from all four bacterial genera, including hosts with no detectable symbiont in genome assemblies. Taken together with these discoveries support the existence of a stable and limited network of four possible nutritional symbiont lineages with rare evidence of symbiont turn-overs. Significance statementTriatominae bugs, vectors of Chagas disease, are known to harbor a diverse community of nutritional bacterial symbionts whose genomic and metabolic roles have remained largely unexplored. By reconstructing 15 symbiont genomes that segregate as four bacterial genera, we provide important insight into the origins, the evolution and the metabolic structure of the nutritional symbiosis in triatominae. These findings support a stable, evolutionary conserved network of nutritional symbionts with limited turnover.

The ability of the bacterial endosymbiont Wolbachia pipientis to block arboviruses in its mosquito host may be impinged by host genetic variation, leading to reduced efficacy in field releases. Across a large collection of Drosophila lines carrying natural genetic variation, we found that viral replication varied greatly in the absence of Wolbachia. However, the introduction of the symbiont reduced viral load in each background to similar levels, near the limit of detection. Therefore, Wolbachia-mediated viral blocking is seemingly robust against host genetic background. A genome-wide association study harnessing the variation in the viral loads across the Wolbachia-free set identified rhoGAP18B and betaCOP as host factors that contribute to SINV replication; furthermore, the gene products of which seemingly interact with each other in the context of cytoskeletal dynamics. These results shed light on host requirements for SINV replication and suggest possible avenues by which Wolbachia may encroach upon them during blocking.

Returning individualized microbiome results in ways that are ethical, comprehensible, and useful remains under-explored in African settings. We nested a multi-site, mixed-methods study within the AWI-Gen Wave 2 gut microbiome sub-study of 1,801 women aged 42 to 86 years to engage the participants and provide feedback. All (1,001) participants from Agincourt and Soweto (South Africa) and Nairobi (Kenya) were invited to feedback meetings: 496 from Agincourt, 87 from Soweto, and 195 from Nairobi responded. Engagement strategies were tailored by site (small-group and home-based sessions, visual metaphors, Foldscopes, and local-language delivery). Using semi-structured discussions and structured observations analysed thematically in MAXQDA under COREQ, five cross-cutting themes emerged: (1) understanding of microbiome reports, (2) emotional responses to feedback, (3) perceived health relevance, (4) trust in research institutions, and (5) suggestions for improving engagement. Culturally grounded explanations and local-language facilitation enhanced comprehension and perceived relevance; English-heavy sessions were associated with more confusion. Most participants expressed satisfaction and described planned or enacted dietary and lifestyle changes, while frustration centred on long delays between sampling and feedback. Trust increased with transparency and individualized return of results but was often conditional on minimizing burdensome procedures such as repeat blood sampling (phlebotomy) and ensuring timely feedback. Engagement was feasible and low-cost (approximately USD 29-59 per participant) with site-specific resource needs. Limitations included constrained generalizability beyond the three study sites. Returning individualized microbiome findings in community settings in Africa is acceptable, feasible, and can motivate health-promoting behaviours when delivered promptly and in culturally and linguistically appropriate ways.

AbstractMicrobial diversity is often assumed to be limited by the number of available resources, yet many communities persist well beyond that expectation. Understanding the mechanisms that enable such coexistence remains a central question in microbial ecology. Here, using a four-species bacterial consortium, we asked whether coexistence can emerge from interactions between species rather than from the external environment alone. Across 31 simple nutrient conditions, including 16 single-resource environments, all four species persisted and repeatedly reached stable coexistence. We then chose 27 additional conditions to further probe the boundaries of coexistence by varying resource concentrations, temporal dynamics, nutrient complexity and relief of auxotrophy-associated dependencies, and only observed the extinction of one species in one of these conditions. Although the community composition in each environment was largely shaped by species fitness on the supplied resources, experimental assays and consumer-resource modeling showed that the coexistence was not explained by resource supply, but rather by cross-feeding and niche partitioning of metabolic byproducts. These metabolic interactions were strong enough to sustain coexistence even for species unable to use the supplied resources directly. Furthermore, robust coexistence across environments appears to be an emergent property of microbial communities, ingrained in members metabolic byproduct profiles and niche differences. Our findings demonstrate how microbes can increase the chemical complexity of their environment sufficiently to maintain coexistence well beyond what is expected from external resource supply. SignificanceUnderstanding the drivers of microbial diversity is essential for managing natural ecosystems and designing synthetic microbiomes. This study challenges the conventional application of the competitive exclusion principle, demonstrating that a four-species consortium can coexist across 31 chemically and metabolically diverse one- and two-carbon source environments. By systematically testing and ruling out alternative stabilizing mechanisms, we show that co-existence is an emergent property of the consortium, sustained by metabolic cross-feeding and niche partitioning. Guided by computational models, we identify hallmarks of robust co-existence in simple environments, including high variance in resource affinities and growth on partner-derived metabolites. Our work demonstrates how microbes modify their environment to sustain high diversity and provides principles for designing synthetic microbiomes that persist across environments.

Neural correlates of consciousness are often evaluated along single dimensions, such as large-scale integration or metabolic activity, yet it remains unclear whether either is sufficient, or whether conscious states require the joint satisfaction of multiple biological constraints. Here, we evaluate the prediction that conscious states occupy a regime defined by the co-occurrence of sufficient metabolic support and preserved perturbational complexity. We performed a targeted cross-study synthesis of published benchmarks from [18F]-fluorodeoxyglucose positron emission tomography (FDG-PET) and transcranial magnetic stimulation combined with electroencephalography (TMS-EEG). Metabolic values and perturbational complexity index (PCI) values were mapped across disorders of consciousness, sleep, and anaesthesia into a shared two-dimensional state space. Across independent cohorts, a lower bound near ~42-46% of normal cortical metabolism and a complexity threshold near PCI* {approx} 0.31 consistently separate unconscious from conscious conditions. Of 16 conditions with complete data, all 9 conscious states occupied the joint regime (above both thresholds), while all 7 unconscious states fell below at least one threshold (Fishers exact test, p = 8.74 x 10-5). The sole off-diagonal placement -- NREM sleep, with preserved metabolism but reduced complexity -- was unconscious, supporting the prediction that metabolic support alone is insufficient without preserved integrative dynamics. These findings support a joint metabolic-integrative constraint on consciousness and motivate a testable prediction: reportable experience should not occur outside this regime. Direct evaluation will require prospective within-subject multimodal studies combining FDG-PET and TMS-EEG.

Neural circuit assembly relies on different neuronal subtypes coming together to form a functional circuit. The question of how the appropriate number of each subtype is integrated into an emerging circuit remains relatively unknown. To answer this question, we used the mouse retina to uncover the molecular mechanisms responsible for neuron subtype integration in a developing circuit. In the mammalian retina, bipolar neurons are a class of interneurons that relay visual information from photoreceptors to ganglion cells. Extensive studies have shown there are 15 distinct bipolar subtypes: 6 types of OFF cone bipolars, 8 types of ON cone bipolars, and 1 type of rod bipolar. During retinal development, bipolar neurons are born in excess and through programmed cell death, a precise number of each subtype remains to give rise to the retinal circuit. Although this process has been well-described, little is known about the key molecules responsible for bipolar subtype integration in the developing retina. Our work uncovered a new role for the autism-associated risk gene, Protocadherin 9 (Pcdh9) in bipolar subtype integration. Deletion of Pcdh9 using a floxed allele leads to loss of OFF and ON cone bipolars; however, disruption in the extracellular binding of Pcdh9 leads to selective loss of ON cone bipolars but not rod bipolars. Moreover, we found this later function of Pcdh9 is mediated by homophilic interactions between ON cone bipolars and their known synaptic partners. Taken together, our work revealed a new role for Pcdh9 in bipolar subtype integration during retinal development. SUMMARY STATEMENTNeural circuits are comprised of multiple neuronal subtypes where a specific number need to come together to give rise to a functional circuit. Although this is a critical process during neurodevelopment, little is known about the molecular mechanisms that determines the precise number of each subtype during circuit development. In the present study, we identified the autism risk gene, Protocadherin 9 as a critical molecule in subtype integration of bipolar neurons within the developing mouse retina. Using newly generated mouse lines, we found distinct requirements of Pcdh9 to promote survival in different bipolar subtypes during retinal circuit assembly. The significance of this work is that it shed lights into how different neuronal subtypes are integrated in nascent neural circuits.

The central role of microglia in CNS function in health and disease has resulted in large interest in targeting microglial as treatments for neurodegenerative disease; understanding the factors that regulate microglial gene expression will be crucial to this goal. microRNAs (miRNAs) are among the most abundant post transcriptional regulators of gene expression. miRNAs suggests miRNA were likely key to significant evolutionary events as regulators of gene expression. The miRNAome of microglia is critical to their correct functioning but the miRNA that define microglia identity and regulate key functions have not been fully defined. In this study we performed a detailed analysis of the microglial miRNAome to identify miRNA enriched in microglia that are conserved across species (human, mouse, and xenopus). We further characterised the expression of these conserved miRNAs during demyelination and remyelination and identified conserved function of a microglial-enriched miRNA across species. These findings reveal evolutionary conservation of specific miRNAs, suggesting an important role in establishing and maintaining microglial identity. They also highlight miRNAs that may be critical for microglial function in the central nervous system in both health and disease. Overall, this work advances our understanding of the factors that regulate microglial gene expression.

Cooperators that pay a cost to provide benefits to others are vulnerable to exploitation by defectors that reap the benefits while avoiding the costs. Thus selection on the individual level can lead to loss of cooperators while lowering overall population fitness. Accordingly, the maintenance of cooperation is a key problem in evolutionary biology. The puzzle of cooperation extends to viruses: cooperative viruses produce gene products that can be shared, while defector viruses produce less and instead use products made by cooperators. In coinfection, defectors are always advantaged, predicting the loss of cooperation. However, the fitness of cooperator and defector phenotypes is context dependent. Though defectors are advantaged in coinfection, they suffer reduced replication in single infections. Environmental feedback is the process by which changes in population composition alter viral densities and rates of coinfection, which in turn feed back to affect the fitness of each type. We show that environmental feedback maintains cooperation in viruses. We also find that defector emergence may interfere with phage therapy by disrupting the phage dynamics that cause host extinction, and demonstrate that the introduction of defectors lowers viral densities and drives viral extinction, suggesting that defectors that replicate alone could function as antiviral therapies.

The spatial configuration of habitat patches is a key driver of metacommunity dynamics, yet the role of network topology remains poorly understood. In this study, I experimentally tested how different aspects of network structure influence metacommunity processes operating at different spatial scales. Using protist microcosms, I assembled metacommunities with patches connected as random or scale-free networks, and quantified occupancy, biomass, and extinction dynamics in relation to local (patch degree) and global (closeness centrality) metrics of connectivity. Scale-free metacommunities supported higher occupancy and biomass than random networks. At local scales, biomass declined with increasing patch degree, suggesting that reduced connectivity may enhance productivity, likely by limiting negative interactions. In contrast, extinction dynamics were not related to degree but strongly associated with patch centrality, with network topology modulating the relationship. These results reveal a decoupling between ecological processes, showing that different components of network structure can regulate dynamics at different spatial scales.

O_LIFloral polymorphisms frequently persist across heterogeneous environments despite ongoing gene flow, yet the regulatory mechanisms maintaining discrete phenotypes remain unclear. We tested whether alternative flower-colour morphs in Stellera chamaejasme L. are maintained by canalized gene regulatory architectures that stabilize expression around morph-specific optima. C_LIO_LIWe used a pan-transcriptomic and eco-evolutionary framework integrating genome-wide gene expression profiling, co-expression network analysis, functional enrichment, ortholog-based phylogenomics, and variance-based modeling of regulatory canalization and transgressive expression to quantify regulatory variation across morphs. C_LIO_LITranscriptomic variation was structured primarily by morph identity rather than geography, indicating consistent morph-associated regulatory programs. Parental morphs showed reduced within-morph variance in gene co-expression modules, consistent with strong regulatory constraint at the network level. In contrast, a naturally occurring mosaic morph exhibited extensive non-additive and predominantly transgressive expression, with most genes falling outside the parental range. This transgressive signal was modular, with most networks remaining stable while a subset showed elevated variance and disrupted inheritance. Functional analyses further reveal that floral pigmentation is embedded within broader metabolic and stress-response pathways, linking color polymorphism to coordinated physiological states and ecological differentiation. C_LI

CRISPR-Cas are widespread adaptive immune systems that protect bacteria and archaea from mobile genetic elements such as bacteriophages. Metagenomic sequencing identified CRISPR-Cas systems in phage genomes; however, their functions remain largely unknown. Here, we present Cas12r-CRISPR, a novel type V CRISPR-Cas system encoded by Lalka phages infecting thermophilic Thermus bacteria. We determined Cas12r-CRISPR PAM consensus sequence and crRNA structure and showed, that when provided with appropriate spacers and expressed in Thermus thermophilus, Cas12r-CRISPR efficiently interferes with plasmid transformation as well as infection by diverse Thermus phages. In the course of Lalka phage infection, the Cas12r-CRISPR locus is expressed with middle phage genes and its transcripts are among the most abundant phage RNAs. Notably, most Cas12r-CRISPR spacers target integrative mobile elements widespread in Thermus genomes. Both Lalka phages and targeted integrative mobile elements use host tRNA genes as attachment sites. We therefore propose that Cas12r-CRISPR participates in an inter-MGEs conflict. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=81 SRC="FIGDIR/small/719267v1_ufig1.gif" ALT="Figure 1"> View larger version (23K): org.highwire.dtl.DTLVardef@13f66f7org.highwire.dtl.DTLVardef@180fa5corg.highwire.dtl.DTLVardef@b4e527org.highwire.dtl.DTLVardef@30950b_HPS_FORMAT_FIGEXP M_FIG C_FIG

Abrupt regime shifts of complex ecosystems between alternative stable states are widespread in nature. Yet, our mechanistic understanding of disturbance-shift-ecosystem functioning relationships remains poor, and it is further unclear whether biotic disturbances can drive such shifts. Using a 5-year pond experiment, we demonstrate that invasion by the red swamp crayfish (Procambarus clarkii) drove a regime shift from a clear-water, macrophyte-dominated, to a turbid, phytoplankton-dominated state. The regime shift was associated with increased water temperature due to increased water turbidity enhanced light absorption, and with a seasonal switch of ecosystem metabolism from hetero-to autotrophy due to decreased respiration in summer, despite constant gross primary production. Reducing crayfish population densities by 44 % failed to move ecosystems back towards their initial state and functioning. Our results stress that biotic disturbances may have hardly-reversible consequences on the biophysical and biogeochemical processes that support ecosystem functioning.

Midbrain dopamine (DA) neurons critically regulate basal ganglia function through their widespread projections. While the nigrostriatal pathway is well characterized and represents the dominant source of DA in the basal ganglia, other nuclei such as the external Globus Pallidus (GPe) also receive dopaminergic innervation, yet no consensus exists about its precise anatomical origin. In addition, the GABAergic tail of the ventral tegmental area (tVTA) provides a major inhibitory input to midbrain DA neurons, but its influence over DA pathways to the GPe remains unknown. In the rat, we combined retrograde tracing, immunohistochemistry, and ex vivo electrophysiology to identify distinct populations of DA neurons in the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) that project to the GPe and display distinct electrophysiological properties. Using optogenetics and electrophysiology, we also demonstrate that these GPe-projecting DA neurons receive powerful inhibitory input from the tVTA. Together, our findings define both the origin and inhibitory control of dopaminergic innervation to the GPe, revealing a previously unrecognized disynaptic circuit (tVTA[->]DA[->]GPe) that refines our understanding of basal ganglia circuit function.

Influenza A virus (IAV), as all other viruses, is completely dependent on the host translation machinery components, including host transfer RNAs (tRNAs), to effectively decode its genome. However, while the human genome is biased towards cytosine (C) and guanosine (G)-ending codons, the IAV genome is skewed towards adenine (A) and uridine (U)-ending codons. Nevertheless, translation of IAVs RNA genome is highly efficient. Here we show that host tRNA and tRNA epitranscriptome dynamics are important regulators of IAV RNA translation and host antiviral responses. We show that the levels of several tRNA modifications, including 5-methylcarboxymethyluridine (mcm5U34) and 5-methoxycarbonylmethyl-2-thiouridine (mcm5s2U34), and their cognate writers, vary over the course of IAV infection. Additionally, we demonstrate that a set of tRNAs are preferentially recruited to ribosomes upon IAV infection, in line with IAV codon usage requirements. We further show that loss of ELP3, the catalytic subunit of the elongator complex, which is involved in the catalysis of mcm5U34 and of mcm5s2U34, induces tRNA hypomodifications, impairs translation of codon biased IAV genes and triggers the integrated stress response (ISR), interfering with IAV propagation. Taken together, our results uncover the relevance of host tRNAs and their modifications for optimal expression of viral genomes and host antiviral responses, setting the tRNA epitranscriptome as a promising target for the development of host-based antiviral therapies.

An animals nervous system enables it to detect and respond to stimuli to navigate its environment. To enhance sensory acquisition, animals can actively position sensors, altering how they extract information from the external world. However, active sensing, and movement in general, produces sensory feedback, requiring mechanisms for integrating predictive motor signals with externally generated sensations. Despite the importance of these mechanisms for guiding coordinated behavior, the cellular and circuit basis of motor control and sensory processing during active movements are not fully understood. Here, we investigate how mechanosensory information contributes to motor output in the Drosophila antenna, a sensor that can be actively positioned. We combine electrophysiology, quantitative behavior, optogenetics, and connectomics to characterize APN2, a nonspiking interneuron in Drosophila that encodes both mechanosensory stimuli and motor commands. We show that these neurons receive input from two classes of antennal mechanosensors, enabling responses to mechanical perturbations in both quiescence and flight. We then demonstrate how these neurons integrate higher-order motor commands with mechanosensory input to shape antennal movement. Together, this work reveals a previously uncharacterized sensory-motor circuit in the antennal mechanosensory system. These findings provide insight into how nervous systems integrate sensation with motor commands to guide the movement of active sensors, highlighting circuit mechanisms that may broadly support sensory acquisition during movement.

Recent advances have shown that the complexity of neural signals tracks global states of consciousness, such as wakefulness versus sleep. However, it is still unclear to what extent neural complexity reflects fine-grained changes in conscious content within the same global state. Here, we investigate how the complexity of brain signals is affected by increased perceptual clarity of a stimulus. To this end, we estimated neural signal complexity using Complexity via State-space Entropy Rate (CSER) to EEG recordings from an auditory discrimination task. In this paradigm, auditory stimuli were presented at varying signal-to-noise ratios (SNRs), with higher SNRs corresponding to greater subjective audibility and perceptual clarity, enabling us to relate neural complexity to graded perceptual awareness within a constant global state of consciousness. Our results showed that, while broadband CSER remains constant across SNRs, its spectral decomposition displays frequency-specific effects, with higher SNRs associated with a decreased complexity in and {beta} bands, increased complexity in{delta} , and no significant changes in{gamma} . Additionally, a temporal investigation of CSER exhibited a significant increase in complexity with stimulus clarity, with deviations from baseline peaking approximately 30 ms before the ERP. Extending this analysis to pairs of brain regions, mutual information rate uncovered a sudden post-stimulus breakdown in long-range information transmission relative to baseline. Taken together, these results reveal that while aggregated complexity measures track global states of consciousness, time- and frequency-resolved information-theoretic measures can capture variations in perceptual awareness, demonstrating their sensitivity as estimators of the level of conscious experience.

Human experience unfolds continuously, yet it is remembered and understood as a sequence of discrete events. How the brain segments this stream of experience, particularly under naturalistic conditions, remains poorly understood. Here we investigate the neural dynamics associated with event boundaries during active navigation through architectural transitions. Using mobile electroencephalography combined with virtual reality, we analyzed data from participants freely walking between rooms and repeatedly crossing doorways. Time-frequency analysis of source-localized neural activity revealed a robust increase in theta-band power (4-8 Hz) over temporo-occipital and parietal regions approximately 300-450 ms after passing through a doorway. This effect was consistent across participants and independent component clusters, indicating a reliable neural signature of architectural transitions. We interpret this theta response within frameworks of event segmentation and Bayesian inference, suggesting that doorways trigger a transient reconfiguration of distributed neural networks when ongoing predictions can no longer be maintained and a new event model must be inferred. By preserving the natural coupling between perception, movement, and environmental structure, our findings demonstrate that architecture provides meaningful boundaries that shape brain dynamics and the organization of experience. More broadly, this work highlights the power of naturalistic experimentation and positions architectural space as an active medium for investigating how the brain structures events.

Cellular homeostasis is sustained by balancing the cell growth and quiescence in response to specific environmental cues. While the mechanisms governing the transition from growth to dormancy are reasonably well understood, the processes underlying exit from dormancy remain poorly characterised. Using an integrated approach employing bacterial genetics, Cryo-EM, and molecular microbiology, we investigated this phenomenon by studying the cross-talk between two antagonistic pathways, ribosome biogenesis that promotes cell growth, and stringent response that induces dormancy. We show that the exit from dormancy requires a conserved Era GTPase whose synthesis selectively rises during onset of exponential growth phase in Escherichia coli. Era not only accelerates the maturation of head and platform regions of 30S ribosomal subunit but also dislodges RelA from 70S ribosome. This derepresses the 70S ribosome from RelA-mediated inhibition, and promotes protein synthesis driving the active cell growth. This study uncovers that temporal epistatic interaction between Era and RelA governs cellular resuscitation in bacteria. Given that the dormant bacterial populations contribute to antibiotic tolerance, understanding this regulatory axis offers new insights for resensitising the recalcitrant dormant bacteria to antibiotics.

Food provides nutrients that are selectively absorbed by the intestine, but, at the same time, may contain elements that challenge the intestinal barrier and induce post-prandial inflammation (PPI). How PPI is controlled in order to avoid pathological perturbation of homeostasis remains unclear. Here, we report that during fasting, enterocytes increase their absorptive potential and oxidative metabolism, a program that is largely reversed upon food intake of lipids that perturb the intestinal barrier and induce PPI. Such perturbation is countered by ILC3s, in the absence of which PPI increases, program reversal does not occur, and enterocytes engage into excessive oxidative metabolism. This enterocyte state leads to critical hypoglycemia as a consequence of decreased glucose absorption and increased insulinemia, recapitulating the pathological situation found in patients suffering from intestinal damage and sepsis. We hereby uncover a critical function for ILC3s in maintaining enterocyte homeostasis upon challenging food intake.

A long-standing hypothesis in sensory neuroscience suggests that the evolutionary expansion of cortex in mammals may contribute to sensory-dependent adaptation by acting on subcortical pathways that drive innate behavior. However, direct experimental evidence is lacking. Taking the visual system as a model, it is known that there is significant interaction between the evolutionarily conserved Superior Colliculus (SC) and the comparatively modern Visual Cortex (VC), key structures in the mammalian visual system. In the SC, local alignment is established between a retinotopic map of the visual field and a map of orienting movement vectors during development and drives accurate visually guided orienting behavior throughout an organisms lifespan. Interestingly mammals, like humans and non-human primates, readily adapt to altered visual experiences, while evolutionarily older vertebrates, like amphibians, lack this behavioral plasticity. To address this outstanding question, we have developed a novel behavioral paradigm for inducing visuomotor adaptation in freely moving mice that is analogous to paradigms utilized in primates. Our paradigm combines a visually guided orienting task and a novel mouse prism goggle system to shift the visual field. Using this paradigm, we demonstrate for the first time that mice gradually adapt to a chronic shift of their full visual field, suggesting this type of behavioral plasticity is conserved across mammalian species. Furthermore, we show that lesioning primary visual cortex (V1) prior to shifting the visual field disrupts normal visuomotor adaptation, suggesting that VC may play a generative role in the plasticity of fundamental visually guided behaviors. These findings lend support to the hypothesis that a particular evolutionary benefit of sensory cortex is the allowance for experience-dependent behavioral plasticity.