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Tian, D.

Publications and source records attributed to Tian, D..

At least 19 recordsLinked to original sources

Rescued from extinction in two buckets: genomic consequences of an extreme bottleneck in the endangered Owens pupfish

Rapid population bottlenecks can threaten population viability by reducing genetic diversity and effective population size while increasing inbreeding. Freshwater fishes are particularly vulnerable to bottlenecks due to habitat fragmentation, water extraction, and invasive species. The Owens pupfish (Cyprinodon radiosus) is an endangered freshwater fish endemic to Owens Valley, CA that was originally thought to be extinct prior to rediscovery in 1964. In 1969, Edwin (Phil) Pister famously saved the entire species from extinction in two buckets after learning that the sole spring they inhabited was drying up. Today, six extant refuge populations ranging in size from 100 - 10,000 individuals remain, which all descend from this severe bottleneck of an estimated 400 individuals. Here, we sequenced whole genomes of 12 individuals from two populations (one extirpated, one extant) to reconstruct recent demographic history and examine the genomic consequences of this well-documented bottleneck on genetic diversity, effective population size, and inbreeding in the Owens pupfish. We estimated the timing of the bottleneck precisely to 1977-1985, closely coinciding with its documented history. Genetic diversity is low across the genome and the bottleneck caused a 17-fold contraction in effective population size over the span of 8 generations. We found low levels of inbreeding that likely predated the bottleneck. Our results suggest that Owens pupfish are threatened by reduced genetic diversity and low effective population size which may constrain adaptive potential, but that recent inbreeding is unlikely to be a serious concern due to population expansion. Our study highlights how the long-term effects of bottlenecks depend not only on severity, but also duration and the rate of population growth afterwards.

evolutionary biology↗

Degraded neural representations foreshadow failures of sustained attention

Attention prioritizes relevant information from the environment, but does not do so consistently over time. Instead, we sometimes experience poor attentional states which are characterized by a higher degree of performance failures, or "lapses." The source of these lapses--whether they arise from attentional disengagement, failures of attentional selection, or simply failures of response control--is not clear. This study tests whether the strength of neural representations differs as a function of both attentional selection and modulation over time. We recorded electroencephalography (EEG) data while participants performed a sustained attention task requiring the selection of task-relevant items and withholding of responses to rare targets. Results show that relevant items receive prioritized processing in brain signals, as measured with EEG decoding. Yet, their neural representational fidelity weakens under poor sustained attentional states, foreshadowing upcoming behavioral failures. These findings support a neural basis of disengagement during poor attentional states, suggesting that lapses may arise from a decoupling of brain activity from task processing. Finally, pre-item representational strength predicted memory success for targets, suggesting that neural fidelity indexes an encoding-ready state. Results suggest that the quality of neural representations is affected by ongoing attention and plays a key role in processing and memory.

neuroscience↗

Regulatory-scale stripe analysis from single-cell Hi-C with scStripe

Chromatin stripes are a directional architectural feature of three-dimensional genome organization, but their analysis in single-cell Hi-C (scHi-C) at regulatory resolution is hindered by extreme sparsity. We developed scStripe, an imputation-free two-stage statistical framework that detects stripes from sparse cell-type--aggregated scHi-C maps and directly quantifies the resulting aggregate-defined stripes in raw individual-cell contact maps using per-cell stripe scores. Across three complementary benchmark settings, scStripe achieved the highest F1 scores and showed strong aggregate stripe enrichment, while the detected stripes recapitulated characteristic structural and regulatory features reported in bulk data. Per-cell stripe scores resolved recurrent configurations of the EBF1-anchored stripe, captured genome-wide variation associated with cell type, cell-cycle phase, and developmental stage, and identified positively associated gene--stripe pairs with pronounced cell-type specificity using matched scRNA-seq. Together, scStripe provides a practical, scalable framework for regulatory-scale stripe analysis across single cells without requiring single-cell enhancement or 3D reconstruction.

genetics↗

DiffDomain-Spectrum identifies structurally reorganized TADs from sparse aggregated single-cell Hi-C contact maps

Structurally reorganized topologically associating domains (TADs) capture condition- or cell-type-specific remodeling of chromatin contacts and are important for understanding genome organization in health and disease. Emerging single-cell Hi-C (scHi-C) technologies enable such comparisons across heterogeneous cell populations, but aggregated scHi-C contact maps remain sparse at biologically meaningful 25 kb resolution, limiting reliable TAD reorganization detection. Here we present DiffDomain-Spectrum, a spectral statistical framework for identifying reorganized TADs between conditions or cell types from aggregated raw scHi-C contact maps. It tests normalized TAD-level difference matrices without separately normalizing sparse maps or enhancing individual scHi-C contact maps. Comparison with a semicircle-law null integrates evidence across the full eigenvalue spectrum. Across multiple scHi-C platforms, DiffDomain-Spectrum balances false positive control and detection sensitivity relative to alternative bulk callers, and detects a substantially higher proportion of reference TADs as reorganized than the boundary-focused single-cell method scHiCluster. Detected TADs show coherent aggregate contact patterns and CTCF binding changes and are enriched for differentially expressed genes, supporting biological relevance. Together, these results establish DiffDomain-Spectrum as a statistically principled framework for comparative domain-level analysis of sparse aggregated scHi-C contact maps without single-cell map enhancement.

genetics↗

Long-term small effective population size, inbreeding, and a recessive lethal haplotype drive premature death in the endangered Devils Hole pupfish (Cyprinodon diabolis)

As anthropogenic habitat fragmentation and population decline accelerate globally, growing numbers of species face compounding demographic and genetic threats to long-term survival. Many populations are already forced to persist at chronically small sizes, yet the genomic and fitness consequences of this fate remain poorly understood. Here we leverage the demographic history of the Devils Hole pupfish to investigate how long-term small population size and recent bottlenecks have shaped genetic diversity, genetic load, inbreeding, and fitness through comparative population genomics, historical sequencing, and sampling embryos that died prematurely during development. We find that genetic diversity in Devils Hole pupfish is among the lowest recorded in the wild and that fixed load is high, consistent with thousands of generations of isolation at small population size. Even in the face of this low diversity and high fixed load, we show that inbreeding is still strongly associated with premature embryonic death, which affects up to 25% of offspring in the captive refuge and can be identified in advance based on a characteristic elongated heart tube and reduced heart rate. We discovered a recessive lethal haplotype segregating at [~]20% frequency that accounts for 50% of embryonic deaths and contains mutations in MIB1 and MMP16, genes associated with cardiomyopathy and atrial fibrillation. Our findings link genotype, phenotype, and fitness in an iconic endangered species to provide a rare comprehensive view into the evolutionary dynamics and consequences of long-term small effective population size, demonstrating that endangered species remain vulnerable to inbreeding depression despite extremely low genetic diversity.

evolutionary biology↗

Global adaptation to climate change in the twilight zone revealed by shared signals of selection in mesopelagic lanternfishes

Rapid accumulation of greenhouse gases threatens humanity and global diversity. The oceans absorb 30% of anthropogenic carbon emissions annually, but adaptation to climate change by the biotic components of this sink are poorly understood. Lanternfishes (Myctophiformes) are the most abundant vertebrates on the planet by biomass and the dominant mesopelagic vertebrate consumers, thus crucial components of the global carbon cycle. However, it is unknown whether lanternfishes are adapting to global warming and ocean acidification (OA). We hypothesized that warming and OA would act as major shared selective forces across diverse oceanic environments and that disparate taxa would respond in parallel through shared genetic pathways. We used whole-genome sequencing to test this hypothesis by identifying shared signals of selection across lanternfishes from multiple sites in the Atlantic and Pacific spanning three genera (Benthosema glaciale, Triphoturus mexicanus, and Diaphus theta). Across all species we found evidence of expansion from a population bottleneck possibly corresponding to the last glacial maximum and effective population sizes of only 5 million, suggesting substantial reproductive skew and spatially restricted populations. We successfully identified 34 candidate genes experiencing strong shared selection pressure across all taxa in both oceans. 81% of these candidate genes were consistent with adaptations to warming and OA, including a heat-shock protein (HSP70) and genes related to skeletal development, calcium homeostasis, and biomineralization. 14 out of 34 candidate genes are also known from experimental climate change studies to be involved in the response to hypoxia, altered pH, and thermal stress. We found significant gene ontology enrichment within these candidates for otolith morphogenesis, a major component of OA adaptation in fishes. This study provides a new approach for studying climate change adaptation at a global scale and our results imply widespread shared adaptive responses of marine species to climate change.

evolutionary biology↗

Indirect genetic effects across ontogeny in an avian cooperative breeder

Social interactions are ubiquitous in nature and have the potential to affect trait evolution, particularly in group-living animals such as cooperative breeders. Interactions among conspecific individuals can affect the amount of additive genetic variation for a trait when the phenotype of an individual is also affected by the genotype of its social partner(s) via indirect genetic effects. Thus, quantifying both direct and indirect genetic effects of social partners is critical for understanding and predicting evolutionary trajectories. While much is known about maternal indirect genetic effects, empirical estimates of indirect genetic effects from other social partners remain limited, particularly in wild populations. Here, we use animal models to assess the contribution of indirect genetic effects from all social partners in a family group (mothers, fathers, and helpers) on juvenile morphometric traits across ontogeny in the cooperatively-breeding Florida scrub-jay (Aphelocoma coerulescens). We found indirect genetic effects of helpers and fathers on nestling weight, but no indirect genetic effect of mothers. Across ontogeny, we found increasing additive genetic variation in both weight and tarsus length. Our study provides a comprehensive assessment of within-group indirect genetic effects in a cooperative breeder and highlights the importance of considering indirect genetic effects beyond maternal effects.

evolutionary biology↗

A standardized framework resolves ambiguity in motor neuron loss across neurodegenerative diseases

Motor neuron (MN) loss is a hallmark of neurodegenerative disorders, yet its assessment remains variable, confounding mechanistic and therapeutic interpretation. To address this, we conducted a systematic review and meta-analysis of spinal muscular atrophy (SMA) mouse studies, revealing 60% variability in reported MN loss, largely attributable to nonspecific spinal cord sampling. Using a whole-segment approach with tissue clearing, MN tracing, and multimodal imaging, we confirmed segment-dependent differences in MN counts. Common MN markers (SMI-32, Nissl) lacked specificity, whereas choline acetyltransferase (ChAT) provided robust labeling in murine and human spinal cords. Deep learning-based whole-mount segmentation enabled unbiased MN quantification and validated manual counts. Integrating analysis with computational modeling established segment sampling as a key driver of variability and revealed degeneration patterns: widespread MN loss in amyotrophic lateral sclerosis (ALS), selective MN loss in severe SMA, and preservation in mild SMA models. These findings establish a framework for reproducible MN quantification. HighlightsO_LISpinal cord segment-specific analysis reduces variability and allows accurate MN quantification C_LIO_LIChAT is the most reliable MN marker in murine and human spinal cords C_LIO_LIDeep learning-based segmentation enables unbiased MN quantification in intact spinal cords C_LIO_LIMN degeneration is widespread in ALS but restricted to pools innervating proximal muscles in severe SMA C_LI

neuroscience↗

HIV-producing resting T cells monopolize virus production, associated PANoptosis, and persistence in lymphoid tissue

O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=147 SRC="FIGDIR/small/703840v1_ufig1.gif" ALT="Figure 1"> View larger version (43K): org.highwire.dtl.DTLVardef@167c265org.highwire.dtl.DTLVardef@10ba2beorg.highwire.dtl.DTLVardef@e97e06org.highwire.dtl.DTLVardef@150c07c_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphic:C_FLOATNO In chronic HIV infection, HIV is produced before antiretroviral therapy (ART) by resting CD4+ T cells in lymphoid tissue germinal centers. Virus production is associated with destruction of T cells, follicular dendritic cells (FDCs), and B cells required for humoral immune responses by PANoptosis (apotosis, pyroptosis and necroptosis) mediated by the PANoptosome, a cellular structure that incorporates cell contents and programmed cell death pathways in a nodal latticework that mediates cell emptying and disruption in progressive stages indicated by the numbers. During ART, persistent HIV-producing resting T cells represent an immediate source of virus for infection rebound on treatment interruption. C_FIG Activated CD4+ T cells have long been considered the principal source of HIV production before treatment and reactivated latently infected cells the source of virus rebound on treatment interruption, based largely on studies of peripheral blood T cells. Here we show before ART in the lymphoid tissue reservoir that HIV-producing resting CD4+ T cells are essentially the sole source of virus production in germinal centers. Virus is produced in infection complexes of virus bearing follicular dendritic cells (FDCs) that induce high multiplicity multi-HIV-DNA copy infections in overlying resting T cells. HIV production is associated with destruction by PANoptosis (pyroptosis, necroptosis and apoptosis) of interacting antibody-producing populations of FDCs, T cells and B cells. PANoptosis is mediated by the PANoptosome, visualized and defined here as a cellular structure incorporating cytoplasmic and nuclear contents and programmed cell death pathway components in a nodal latticework that executes cell emptying and disruption. During ART, HIV-producing resting T cells persist in lymphoid tissues when virus is undetectable in peripheral blood. These HIV-producing resting T cells that persist during ART represent an immediate source of virus to reignite infection on treatment interruption and are thus identified as an important new target for functional cure strategies.

microbiology↗

Estimate of the mutation rate in the endangered Devils Hole pupfish provides support for the drift-barrier hypothesis at an outlying extreme

Mutation rates vary by orders of magnitude across eukaryotes. The drift-barrier hypothesis proposes that drift overwhelms selection for lower mutation rates in small populations, leading to higher mutation rates over time due to the gradual accumulation of mutator alleles. Here, we test this hypothesis in one of the smallest long-term isolated populations in the world, the endangered Devils Hole pupfish (Cyprinodon diabolis). We estimated germline mutation rates in adults and embryos that died prematurely using autozygous segments due to recent inbreeding events. Our estimate of 8.09 x 10-9 per base pair per generation was higher than the mean rate for actinopterygian fishes of 5.97 x 10-9 (95% CI: 4.39 x 10-9 - 7.55 x 10-9) but was lower than predicted for such a low effective population size based on a recent meta-analysis of vertebrate mutation rates and similar to species with much larger effective population sizes, contradicting the drift barrier hypothesis. We also found that embryos which died during development had a higher mutation rate than mature adults, potentially reflecting a segregating lethal mutator allele. We analyzed the mutational spectra of germline mutations and found that spectra between embryonic lethal and mature adults were similar and comparable to other fishes, despite environmental differences in temperature, oxygen saturation, and UV exposure. Mutation rates in this endangered species provide new insights into the mechanisms driving mutation rate variation across vertebrates at one extreme of low effective population size in nature.

evolutionary biology↗

Abalone genomics reveals an ancient asymmetry axis and the multifunctionality of the mantle

Gastropod diversification represents one of the most spectacular evolutionary radiations, underpinned by a fundamentally asymmetric body plan and diverse pigmentation patterns. To understand the genetic underpinnings of these cardinal traits, we constructed a chromosome-level genome assembly for the rainbow abalone, Haliotis iris. Integrating systematic genomics, histoembryology, and molecular assays, we uncover an ancient regulatory axis, conserved for over 544 million years, in which the long non-coding RNA lncRNA1 functions as a competing endogenous RNA to shield pitx transcripts from miRNA-mediated degradation, thereby driving the establishment of asymmetric body patterning, including the mantle. Furthermore, we identify a wnt-mitf-tyr cascade as the driver of melanogenesis and demonstrate that the mantle is the primary site of melanin synthesis. Concurrently, we reveal the mantle as a multifunctional organ possessing mechanosensory capabilities. These findings elucidate the ancient genetic toolkit governing trait evolution in gastropods. TeaserA deeply conserved RNA switch directs gastropod body plans and reveals the mantles hidden talents.

genomics↗

Parallel and non-parallel features of adaptive radiation in Yucatan pupfishes

Understanding the extent of parallelism across adaptive radiations remains a central problem in evolutionary biology. We used whole-genome resequencing of 123 individuals to compare the adaptive radiation of Cyprinodon pupfishes in Lake Chichancanab, Mexico, to an independent radiation of San Salvador Island (SSI) pupfishes in the Bahamas, and assess the repeatability of adaptive genetic architecture, sources of adaptive variation, and stages of selection. Despite rapid craniofacial divergence of trophic specialists within 8-15 kya, only two candidate genes (0.5%; 2/426) were shared between Caribbean radiations. Although adaptive introgression played a major role in SSI, we found minimal evidence of adaptive introgression in Chichancanab, likely due to the geographic isolation of this inland lake. Instead, de novo mutations provided a substantial source of adaptive variation (30.6%) for the endemic zooplanktivore, 15 times higher than the endemic scale-eater on SSI. However, in parallel with SSI, we found strong evidence that adaptive divergence occurred in stages, first on regulatory and standing genetic variation, then on de novo and nonsynonymous mutations. Consistent with adaptive variants near opsin and spermatogenesis genes, functional categories unique to Chichancanab, we found greater visual acuity and divergent sperm morphology in lab-reared zooplanktivores relative to generalists using laboratory assays. Consistent with extensive adaptive de novo mutations in WNT10A and rapid diversification of tooth size in the zooplanktivore, we found that experimental inhibition of the Wnt pathway in generalists resulted in narrower oral teeth. We conclude that de novo mutations, not introgression, can drive rapid adaptive radiations in isolated environments.

evolutionary biology↗

Prognosis prediction using autophagy gene expression in osteosarcoma

Defining the transition from localized to metastatic osteosarcoma (OS) before overt dissemination is fundamental for improving survival. However, effective early diagnostic tools remain scarce, largely due to limited exploitation of the pre-metastatic tumor microenvironments own record of molecular barcode exposures encoded in cell-intrinsic stress states. We analyzed autophagy-dependent transcriptional datasets from 139 individuals to develop Auto-RS, a computational classifier that can integrate age and sex to deliver individualized risk management. The prognosis-interpretable features of Auto-RS recapitulate established molecular trajectories of metastasis at the single-cell level, capturing tumor cells intrinsic shift from proliferative to invasive states and revealing cooperative programs among cancer-associated fibroblasts and immune cells. More significantly, Auto-RS can expose chemotherapy vulnerabilities of newer drugs, providing a framework to prioritize therapeutics without direct testing in children. This framework brings a potential inflection point, where metastasis prediction and therapeutic stratification may converge to improve OS outcomes.

cell biology↗

Impacts of projected elevated temperature on estimated chilling accumulation and bud break of rabbiteye blueberries

Climate change poses a significant threat to perennial fruit crops, including blueberries, by altering temperature-dependent developmental processes such as dormancy and bud break. This study investigates the projected impacts of mid-21st century warming on chilling accumulation and phenological development in rabbiteye blueberry (Vaccinium virgatum) cultivars Krewer and Titan. Using downscaled climate projections from 20 global climate models under the RCP 8.5 scenario, we estimated future temperature trends for a key southeastern U.S. blueberry production region. We quantified changes in chilling hours, chilling portions, and freeze event probabilities between historical (1981-2000) and projected (2041-2070) periods. Results indicate a substantial reduction in chilling accumulation--chilling hours decreased by 66.6% and chilling portions by nearly half--alongside a delayed onset and shortened duration of chilling periods. Despite warming, freezing events are still expected during critical phenological windows, potentially increasing frost damage risk. Growth chamber experiments simulating ambient and elevated temperature regimes revealed significant cultivar-specific shifts in the timing and rate of bud break and bloom stages. Logistic models developed from these data provide predictive tools for assessing phenological responses under future climates. These findings highlight the vulnerability of rabbiteye blueberry to climate-induced dormancy disruption and underscore the need for adaptive management strategies and cultivar selection to sustain productivity in a warming climate.

plant biology↗

Auranofin Inhibits Hepatitis E Virus Replication Via Reactive Oxygen Species

Hepatitis E virus (HEV) causes roughly 20 million yearly global infections, and is associated with chronic hepatitis, neurological sequelae and pregnancy-related adverse outcomes that require antiviral therapeutic intervention. While there are currently no approved HEV-specific therapeutics, ribavirin and pegylated interferon, prescribed off-label, are the current standard of care. However, ribavirin resistance and toxicity highlight the unmet clinical need to identify safer, HEV-specific antivirals. Auranofin, an FDA-approved anti-rheumatic drug, displays antiviral activity against several viruses. Therefore, we investigated auranofins potential as an antiviral and its mechanism of action against HEV. We demonstrated that auranofin displays dose-dependent antiviral activity against two genotypes of HEV that cause a significant proportion of human disease, as well as against a ribavirin treatment failure-associated mutant. Because auranofin is known to increase reactive oxygen species (ROS), we investigated the antiviral mechanism of action via treatment with ROS inhibitors. ROS inhibitors reversed auranofin-mediated ROS promotion and antiviral activity, suggesting the observed antiviral effects are mediated by ROS. Furthermore, treatment with a different ROS promotor, D-amino acid oxidase (DAAO), also displays antiviral activity against HEV, which was also reversed by treatment with a ROS inhibitor, suggesting that ROS accumulation alone is antiviral. We also demonstrated that combined treatment with auranofin and ribavirin exhibits synergistic antiviral activity in vitro, which supports repurposing auranofin as an antiviral against HEV, potentially in combination with ribavirin. Overall, this study has important implications in repurposing auranofin as an antiviral against HEV and in delineating the mechanism of action against HEV via ROS. ImportanceHepatitis E virus (HEV) lacks approved antiviral therapies, and off-label treatments are limited by toxicity and emerging resistance. This study identifies the FDA-approved drug auranofin as an effective in vitro inhibitor of HEV, including two globally relevant human-associated genotypes and a ribavirin treatment failure-associated mutant. Auranofins activity highlights the therapeutic potential of host-targeting antivirals, particularly those that promote the generation of reactive oxygen species, in treating HEV infection. These findings support further in vivo investigations of auranofin as a treatment for HEV and suggest that modulating host redox pathways by promoting reactive oxygen species may represent a promising strategy for broad-spectrum antiviral development.

microbiology↗

Olfactory receptor coexpression and co-option in the dengue mosquito

The olfactory sensory neurons of vinegar flies and mice tend to express a single ligand-specific receptor. While this one neuron-one receptor motif has long been expected to apply broadly across insects, recent evidence suggests it may not extend to mosquitoes. We sequenced and analyzed the transcriptomes of 46,000 neurons from antennae of the dengue mosquito Aedes aegypti to resolve all olfactory, thermosensory, and hygrosensory neuron subtypes and identify the receptors expressed therein. We find that half of all olfactory subtypes coexpress multiple receptors. However, coexpression occurs almost exclusively among genes from the same family--among odorant receptors (ORs) or among ionotropic receptors (IRs). Coexpression of ORs with IRs is exceedingly rare. Many coexpressed receptors are recent duplicates. In other cases, the recruitment or co-option of single receptors by multiple neuron subtypes has placed these genes together in the same cells with distant paralogs. Close examination of data from Drosophila reveal rare cases of both phenomena, indicating that the olfactory systems of these two species are not fundamentally different, but instead fall at different locations along a continuum likely to encompass diverse insects.

neuroscience↗

Comparison of Cd concentration in rice grain between OsNramp5 knock-out mutants and OsHAM3-overexpressing line

Cadmium (Cd) is highly toxic and a carcinogen to humans. Rice is prone to absorbing Cd and accumulating it in the grain, which raises health concerns for rice consumers. OsNramp5 is a major transporter for Cd and manganese (Mn) uptake in rice, whereas OsHMA3 is a tonoplast-localized transporter for Cd detoxification. In this study, we compared the efficiency of OsNramp5 knockout mutation and OsHAM3 overexpression in reducing Cd content in the rice grain. The grain Cd content of the OsNramp5 knockout mutants was significantly lower than that of the wild-type rice T5105. However, the OsNramp5 knockout mutants still had much higher grain Cd content than the similar OsNramp5 mutants reported previously or the OsHAM3 overexpression line developed in our previous study. Pyramiding the OsNramp5 mutant allele and the OsHAM3 transgene in a double homozygous line could not further reduce grain Cd content. The OsNramp5 gene in T5105 has a haplotype II promoter, and its knockout mutation partially impairs Mn uptake in rice. Our results demonstrate that OsHMA3 overexpression works more efficiently in generating low-Cd rice grain than OsNramp5 knockout mutation without affecting Mn uptake in rice.

bioengineering↗

Activation of two noncanonical R proteins by an insect effector confers plant immunity to aphid infestation

Molecular characterization of resistance genes is crucial for efficiently understanding and fortifying plant immunity against insect herbivores. Here we report that RMES1A and RMES1B proteins confer resistance to the sorghum aphid Melanaphis sorghi when activated by an insect effector MsEF1. Map-based cloning plus genetic analysis of knockout mutants confirm that RMES1A and RMES1B are both required for aphid resistance. Upon aphid attack, RMES1A and RMES1B expression is elevated in the sclerenchyma cells and vascular bundles of leaves; the two proteins interact with MsEF1 in the exocysts, thus upregulating key defense processes such as reactive oxygen species burst. Structural modeling predicts that RMES1A and RMES1B each carry an ATP binding site and two leucine-rich-repeat domains but lack coiled-coil or Toll/Interleukin-1 receptor/resistance domain, thus likely representing a new type of resistance controlling proteins in plants. Our work reveals new genes and mechanisms for further deciphering and improving plant immunity to insect pests.

genetics↗