Biology subjects

Lee, H.-Y.

Publications and source records attributed to Lee, H.-Y..

18 recordsLinked to original sources

bioRxiv2026

A Modular Chromosomally Integrated Yeast Surface Display Platform for Quantitative Serology and Immune Profiling

Precise quantification of antigen-specific antibodies is essential for assessing immune status and fundamental to both clinical and research settings. However, current serological platforms remain limited in their ability to combine quantitative performance, flexibility, and scalability. Here, we present a chromosomally integrated yeast surface display (YSD) system engineered for stable, quantitative, and scalable antibody profiling. Genomic integration of the YSD cassette supports uniform antigen presentation without continuous selective pressure, reducing variability associated with plasmid-based systems. Two distinct cell-wall anchoring strategies are implemented within a modular synthetic framework that enables rapid, cloning-free strain construction. Coupled with flow-cytometric readout, the system provides sensitive detection of antigen-specific antibodies with single-cell normalization for antigen expression. In addition, the combination of barcoded YSD strain libraries with fluorescence-activated cell sorting and next-generation sequencing enables multiplexed serological profiling across multiple samples and antigens. As a proof of concept, we demonstrate quantitative antibody detection against SARS-CoV-2 and extend the approach to hepatitis virus antigens, highlighting the utility of this platform as a flexible framework for serological assay development and immune profiling.

bioengineering↗

bioRxiv2026

Retrosplenial cortex vulnerability links severe hypoglycemia to cognitive impairment through neuron-microglia crosstalk

Severe hypoglycemia remains a serious adverse effect of insulin therapy in individuals with diabetes and is linked to cognitive decline, yet the mechanisms by which transient metabolic stress leads to persistent neuronal dysfunction remain poorly defined. Using mouse models of acute severe hypoglycemia and integrated screening, we identified the retrosplenial cortex as a previously unrecognized brain region that is particularly vulnerable to hypoglycemia-induced neuronal damage. This injury is driven by a feedforward interaction between neuron-specific Drp1-dependent mitochondrial fission and microglial IL-1 signaling, as pharmacological or genetic targeting of either pathway suppressed the other, rescued neuronal damage, and reversed cognitive impairment. These findings identify a region-specific neuron-microglia injury circuit that links severe hypoglycemia to cognitive dysfunction and suggest a therapeutic strategy to protect brain function without compromising diabetes management.

neuroscience↗

bioRxiv2025

Antigen reactivity defines tissue-resident memory and exhausted T cells in tumours

CD8+ T cells are a key weapon in the therapeutic armamentarium against cancer. While CD8+CD103+ T cells with a tissue-resident memory T (TRM) cell phenotype have been favourably correlated with patient prognoses1-6, the tumour microenvironment also contains dysfunctional exhausted T (TEX) cells that exhibit a myriad of TRM-like features, leading to conflation of these two populations. Here, we deconvolute TRM and TEX cells within the intratumoural CD8+CD103+ T cell pool across human cancers, ascribing markers and gene signatures that distinguish these CD8+ populations and enable their functional distinction. We found that while TRM cells exhibit superior functionality and are associated with long-term survival post-tumour resection, they are not associated with responsiveness to immune checkpoint blockade. Deconvolution of the two populations showed that tumour-associated TEX and TRM cells are clonally distinct, with the latter comprising both tumour-independent bystanders and tumour-specific cells segregated from their cognate antigen. Intratumoural TRM cells can be forced towards an exhausted fate when chronic antigen stimulation occurs, arguing that the presence or absence of continuous antigen exposure within the microenvironment is the key distinction between respective tumour-associated TEX and TRM populations. These results suggest unique roles for TRM and TEX cells in tumour control, underscoring the need for distinct strategies to harness these T cell populations in novel cancer therapies.

immunology↗

bioRxiv2025

NADPH oxidase inhibitor enhances brain resilience in Alzheimer's disease by reducing tauopathy and neuroinflammation

Alzheimers disease associates closely with activation of NADPH oxidase (Nox) isozymes. We identified that CRB-2131, a novel oxadiazole derivative, potently suppresses Nox isozymes. It inhibits reactive oxygen species production (ROS) by hippocampal neuronal and microglial cells and reduces microglial activation. Prophylactic (starting at 3.5 months of age) and therapeutic (starting at 6 months of age) oral administration with CRB-2131 for 10 weeks in 5XFAD mice reduced hippocampal superoxide levels, lipid peroxidation, Tau phosphorylation, and neuroinflammation. Prophylactic and therapeutic CRB-2131 treatment of 5XFAD mice restored their impaired cognition as shown by the novel-object recognition, Y-maze, and Morris water-maze tests. CRB-2131 treatment increased mature neurons, reduced apoptotic mature neurons, and elevated immature neurons in the hippocampus. Positron-emission tomography/computed-tomography imaging confirmed that CRB-2131 stimulated neuronal regeneration. CRB-2131 suppresses brain oxidation, tauopathy, and neuroinflammation, thereby preventing mature neuron death and promoting neuron regeneration. Ultimately, this fosters a resilient brain and protects cognition.

neuroscience↗

bioRxiv2024

GluN2B-mediated regulation of silent synapses for receptor specification and addiction memory

Psycho-stimulants including cocaine elicit stereotyped, addictive behaviors. Re-emergence of silent synapses containing only NMDA-type glutamate receptors (NMDARs) is a critical mediator of addiction memory and seeking behaviors. Despite the predominant abundance of GluN2B-containing NMDARs in silent synapses, their operational mechanisms are not fully understood. Using conditional depletion/deletion of GluN2B at D1-expressing accumbal medium spiny neurons, we examine the synaptic and behavioral actions that silent synapses incur after repeated exposure to cocaine. GluN2B ablation reduces the proportion of silent synapses, but some of them can persist by substitution to GluN2C, which drives the aberrantly-facilitated synaptic incorporation of calcium-impermeable AMPA-type glutamate receptors (AMPARs). The resultant precocious maturation of silent synapses impairs addiction memory but elevates locomotor activity, which can be normalized by blockade of calcium-impermeable AMPAR trafficking. Collectively, GluN2B supports the competence of cocaine-induced silent synapses for specifying subunit composition of AMPARs, and thereby expression of addition memory and the related behaviors.

neuroscience↗

bioRxiv2023

Oomycete effector AVRblb2 targets cyclic nucleotide-gated channels through calcium sensors to suppress pattern-triggered immunity

Transient, rapid increase of cytosolic Ca2+ upon pathogen infection is essential for plant pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). Several cyclic nucleotide-gated channels (CNGCs) have been implicated; however, their regulatory mechanisms remain elusive. Here, the Phytophthora infestans RXLR effector AVRblb2 family targeted NbCNGC18-20 at the plasma membrane, inhibiting Ca2+ influx and PTI. AVRblb2 required calmodulin (CaM) and calmodulin-like (CML) proteins as co-factors to interact with N. benthamiana CNGCs (NbCNGCs), forming the AVRblb2-CaM/CML-NbCNGCs complex. After recognizing PAMPs, NbCNGC18 formed active heteromeric channels with other CNGCs, potentially providing selectivity for diverse signals to fine-tune cytosolic Ca2+ levels and responses. AVRblb2 suppressed the Ca2+ influx and oxidative burst induced by NbCNGC18 heteromeric complexes. Silencing CNGC18, CNGC20, and CNGC25 compromised the effect of AVRblb2 on P. infestans virulence, confirming that AVRblb2 contributed to virulence by targeting CNGCs. Our findings delineated the regulatory mechanism and role of effector-targeted Ca2+ channels in plant innate immunity.

plant biology↗

bioRxiv2022

The Phytophthora capsici RxLR effector CRISIS2 has roles in suppression of PTI and triggering cell death in host plant

Pathogen effectors can suppress various plant immune responses, suggesting that they have multiple targets in the host. To understand the mechanisms underlying plasma membrane-associated and effector-mediated immunity, we performed Phytophthora capsici RxLR cell death Inducer Suppressing Immune System (CRISIS) screening. In Nicotiana benthamiana, the cell death induced by the RxLR effector CRISIS2 is inhibited by the irreversible plasma membrane H+-ATPase (PMA) activator fusicoccin. Biochemical and gene silencing analyses revealed that CRISIS2 physically and functionally associates with PMAs and induces host cell death independent of immune receptors. CRISIS2 induces apoplastic alkalization by suppressing PMA activity via its association with the C-terminal regulatory domain of PMA. In planta expression of CRISIS2 significantly enhanced the virulence of P. capsici, whereas host-induced gene silencing of CRISIS2 compromised disease symptom and biomass of P. capsici. Furthermore, co-immunoprecipitation assays revealed that CRISIS2 constitutively associates with BAK1, the co-receptor of pattern recognition receptors (PRRs). CRISIS2 interferes with the FLS2-BAK1 complex induced by flagellin perception and impairs downstream signaling from the PRR complex. Proteomics and gene silencing assays identified putative PRRs that negatively regulate the virulence of P. capsici in N. benthamiana as interactors of CRISIS2 and BAK1. Our study identified a novel RxLR effector playing multiple roles in the suppression of plant defense and induction of cell death to support the pathogen hemibiotrophic life cycle in the host plant.

plant biology↗

bioRxiv2021

Inhibition of Ras1-MAPK pathways for hypha formation by novel drug candidates in Candida albicans

The opportunistic human fungal pathogen Candida albicans has morphogenesis as a virulence factor. The morphogenesis of C. albicans is closely related to pathogenicity (1). Ras1 in C. albicans is an important switch in the MAPK pathway for morphogenesis (2, 3). The MAPK pathway is important for the virulence, such as cell growth, morphogenesis, and biofilm formation (4, 5). Ume6 is a well-known transcriptional factor for hyphal-specific genes (6). Despite numerous studies, as a recent issue, it is necessary to develop a new drug that uses a different pathway mechanism to inhibit resistant C. albicans strains caused by chronic prescription of azole or echinocandin drugs, which are mainly used. Here, we show that the small carbazole derivatives attenuated the pathogenicity of C. albicans through inhibition of the Ras1/MAPK pathway. We found that the small molecules inhibit morphogenesis through repressing protein and RNA levels in Ras/MAPK related genes including UME6 and NRG1. Furthermore, we found the antifungal effect of the small molecules in vivo using a candidiasis murine model. We anticipate our findings are that the small molecules are the promising compounds for the development of new antifungal agents for the treatment of systemic candidiasis and possibly for other fungal diseases. Author summaryThe infection by the opportunistic human fungal pathogen Candida albicans occurs mainly in immunocompetent and immunocompromised humans, such as AIDS patients, immunosuppressant-treated organ transplant patients, and recent COVID-19 patients. Morphogenesis which the ability to switch between yeast and hyphal growth forms is one of the representative virulence factors of C. albicans. Here, we describe novel small molecules that show antifungal effects such as the inhibition of the morphogenesis and the biofilm formation, and maintenance of biofilm. Moreover, we found that these small molecules had antifungal activity in mouse experiments, and confirmed that they were also effective in drug-resistant C. albicans strains. Studies of some small molecules with structures similar to ours have already been reported to exhibit growth inhibitory activity against bacteria and Candida species. However, the mechanism of action of these molecules has not been elucidated. In this study, we demonstrated, for the first time, the mechanism by which these two small molecules inhibit C. albicans pathogenicity through inhibition of specific pathways. Our study, through the research of the mechanism of action of novel small molecules, provides new insights into the development of drug candidates not only for wild-type C. albicans, but also for strains resistant to existing drugs.

microbiology↗

bioRxiv2020

Plant NLR targets P-type ATPase for executing plasma membrane depolarization leading to calcium influx and cell death

Hypersensitive response (HR) is a robust immune response mediated by plant nucleotide-binding and leucine-rich repeat receptor (NLR). However, the early molecular event linking NLR to cell death is obscure. Here we demonstrate that NLR targets plasma membrane H+-ATPases (PMA) generating electrochemical potential across the membrane. CCA309, an autoactive N-terminal domain of pepper coiled-coil NLR (CNL), associates with PMAs and its autoactivity is affected by silencing or overexpression of PMA. CCA309-induced extracellular alkalization accompanied with membrane depolarization is followed by calcium influx and cell death. CCA309 interacts with C-terminal regulatory domain of PMA and 14-3-3 negatively affects CCA309-induced cell death. Moreover, pharmacological experiments with fusicoccin, an irreversible PMA activator, confirmed that CC- and CNL-mediated cell death occurred through inhibiting PMA. We propose PMAs as the primary target of plasma membrane-associated CNL to disrupt electrochemical homeostasis leading to HR cell death.

plant biology↗

bioRxiv2020

Impaired hand dexterity function in a non-human primate model with chronic Parkinson's disease

Symptoms of Parkinsons disease (PD) caused by loss of dopaminergic neurons are accompanied by movement disorders, including tremors, rigidity, bradykinesia, and akinesia. Non-human primate (NHP) models with PD play an essential role in the analysis of PD pathophysiology and behavior symptoms. As impairments of hand dexterity function can affect activities of daily living in patients with PD, research on hand dexterity function in NHP models with chronic PD is essential. Traditional rating scales previously used in the evaluation of animal spontaneous behavior were insufficient due to factors related to subjectivity and passivity. Thus, experimentally designed applications for an appropriate apparatus are necessary. In this study, we aimed to longitudinally assess hand dexterity function using hand dexterity task (HDT) in NHP-PD models. To validate this assessment, we analyzed an alteration in Parkinsonian tremor symptoms, loss of dopaminergic neuron, and positron emission tomography (PET) imaging of dopamine transporters (DAT) in these models. HDT latency significantly increased in NHP-PD models. In addition, a significant inverse correlation between HDT and DAT was identified, but no local bias was found. The correlation with intention tremor symptoms was lower than the resting tremor. In conclusion, the evaluation of HDT may reflect behavioral symptoms of NHP-PD models. Furthermore, HDT was effectively used to experimentally distinguish intention tremors from other tremors.

neuroscience↗

bioRxiv2020

CCM 1 determines YAP/TAZ signaling dependent metastatic hallmarks of prostate cancer cells

Enhanced Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ) signaling is correlated with the extraprostatic extension of prostate cancer. However, the mechanism by which YAP/TAZ signaling becomes hyperactive and drives prostate cancer progression is currently unclear. In this study, we demonstrated that CCM1 induces the metastasis of multiple types of prostate cancer cells by regulating YAP/TAZ signaling. Mechanistically, CCM1, a gene mutated in cerebral cavernous malformation, suppresses DDX5, which regulates the PLK1-mediated suppression of YAP/TAZ signaling, indicating that CCM1 and DDX5 are novel upstream regulators of YAP/TAZ signaling. We also revealed that higher expression of CCM1, which is uniquely found in advanced prostate cancer, is inversely correlated with metastasis-free and overall survival in patients with prostate cancer. Our findings highlight the importance of CCM1-DDX5-PLK1-YAP/TAZ signaling in the metastasis of prostate cancer cells. Statement of SignificanceOur analysis of CCM1 expression and function represents a candidate predictive biomarker for prostate cancer metastasis and provides an evidence that abnormality of CCM1 can be pathogenic in prostate cancer. Importantly, CCM1 regulation of metastasis progression appears to a common molecular event in metastatic prostate cancer cells arising in disparate genetic backgrounds.

cancer biology↗

bioRxiv2020

Comparative analysis of seven short-reads sequencing platforms using the Korean Reference Genome: MGI and Illumina sequencing benchmark for whole-genome sequencing

BackgroundMGISEQ-T7 is a new whole-genome sequencer developed by Complete Genomics and MGI utilizing DNA nanoball and combinatorial probe anchor synthesis technologies for generating short reads at a very large scale - up to 60 human genomes per day. However, it has not been objectively and systematically compared against Illumina short-read sequencers. FindingsBy using the same KOREF sample, the Korean Reference Genome, we have compared seven sequencing platforms including BGISEQ-500, MGISEQ-T7, HiSeq2000, HiSeq2500, HiSeq4000, HiSeqX10, and NovaSeq6000. We measured sequencing quality by comparing sequencing statistics (base quality, duplication rate, and random error rate), mapping statistics (mapping rate, depth distribution, and %GC coverage), and variant statistics (transition/transversion ratio, dbSNP annotation rate, and concordance rate with SNP genotyping chip) across the seven sequencing platforms. We found that MGI platforms showed a higher concordance rate of SNP genotyping than HiSeq2000 and HiSeq4000. The similarity matrix of variant calls confirmed that the two MGI platforms have the most similar characteristics to the HiSeq2500 platform. ConclusionsOverall, MGI and Illumina sequencing platforms showed comparable levels of sequencing quality, uniformity of coverage, %GC coverage, and variant accuracy, thus we conclude that the MGI platforms can be used for a wide range of genomics research fields at approximately half the cost of the Illumina platforms.

bioinformatics↗

bioRxiv2020

Calsyntenin-3 directly interacts with neurexins to orchestrate excitatory synapse development in the hippocampus

Calsyntenin-3 (Clstn3) is a postsynaptic adhesion molecule that induces presynaptic differentiation via presynaptic neurexins (Nrxns), but whether Nrxns directly bind to Clstn3 has been a matter of debate. Here, we show that {beta}-Nrxns directly interact via their LNS domain with Clstn3 and Clstn3 cadherin domains. Expression of splice site 4 (SS4) insert-positive {beta}-Nrxn variants, but not insert-negative variants, reversed the impaired Clstn3 synaptogenic activity observed in Nrxn-deficient neurons. Consistently, Clstn3 selectively formed complexes with SS4-positive Nrxns in vivo. Neuron-specific Clstn3 deletion caused significant reductions in number of excitatory synaptic inputs, and moderate impairment of light-induced anxiety-like behaviors in mice. Moreover, expression of Clstn3 cadherin domains in CA1 neurons of Clstn3 conditional knockout mice rescued structural deficits in excitatory synapses, especially within the stratum radiatum layer. Collectively, our results suggest that Clstn3 links to SS4-positive Nrxns to induce presynaptic differentiation and orchestrate excitatory synapse development in specific hippocampal neural circuits.

neuroscience↗

bioRxiv2020

Presynaptic PTPσ organizes neurotransmitter release machinery at excitatory synapses

Leukocyte common antigen-related receptor tyrosine phosphatases (LAR-RPTPs) are evolutionarily conserved presynaptic organizers. The synaptic role of vertebrate LAR-RPTPs in vivo, however, remains unclear. This study systematically analyzed the effects of genetic deletions of LAR-RPTP genes by generating single conditional knockout (cKO) mice targeting PTP{sigma} and PTP{delta}. Although the numbers of synapses were reduced in cultured neurons deficient in individual PTPs, abnormalities in synaptic transmission, synaptic ultrastructures, and vesicle localization were observed only in PTP{sigma}-deficient neurons. Strikingly, loss of presynaptic PTP{sigma} reduced neurotransmitter release prominently at excitatory synapses, concomitant with drastic reductions in excitatory innervations onto postsynaptic target areas in vivo. However, postsynaptic PTP{sigma} deletion had no effect on excitatory synaptic strength. Furthermore, conditional deletion of PTP{sigma} in ventral CA1 specifically altered anxiety-like behaviors. Taken together, these results demonstrate that PTP{sigma} is a bona fide presynaptic adhesion molecule that controls neurotransmitter release and excitatory inputs.

neuroscience↗

bioRxiv2019

Genome-wide expression analysis of immune receptors in hot pepper reveals an autonomous NLR cluster in higher plants

Plants possess hundreds of intracellular immune receptors encoding nucleotide-binding domain and leucine-rich repeat (NLR) proteins. Autoactive NLRs, in some cases a specific NLR domain, induce plant cell death in the absence of pathogen infection. In this study, we identified a group of NLRs (G10) carrying autoactive coiled-coil (CC) domains in pepper (Capsicum annuum L. cv. CM334) by genome-wide transient expression analysis. The G10-CC-mediated cell death mimics hypersensitive response (HR) cell death triggered by interaction between NLR and effectors derived from pathogens. Sequence alignment and mutagenesis analyses revealed that the intact 1 helix of G10-CCs is critical for both G10-CC- and R gene-mediated HR cell death. The cell death induced by G10-CCs does not require known helper NLRs, suggesting G10-NLRs are novel singleton NLRs. We also found that G10-CCs localize in the plasma membrane as Arabidopsis singleton NLR ZAR1. Extended studies revealed that autoactive G10-CCs are well conserved in other Solanaceae plants, including tomato, potato, and tobacco, as well as a monocot plant, rice. Furthermore, G10-NLR is an ancient form of NLR that present in all tested seed plants (spermatophytes). Our studies not only uncover the autonomous NLR cluster in plants but also provide powerful resources for dissecting the underlying molecular mechanism of NLR-mediated cell death in plants.

plant biology↗

bioRxiv2019

Raptor genomes reveal evolutionary signatures of predatory and nocturnal lifestyles

BackgroundBirds of prey (raptors) are dominant apex predators in terrestrial communities, with hawks (Accipitriformes) and falcons (Falconiformes) hunting by day, and owls (Strigiformes) hunting by night.\n\nResultsHere, we report new genomes and transcriptomes for 20 species of birds, including 16 species of birds of prey, and high-quality reference genomes for the Eurasian eagle-owl (Bubo bubo), oriental scops-owl (Otus sunia), eastern buzzard (Buteo japonicus), and common kestrel (Falco tinnunculus). Our extensive genomic analysis and comparisons with non-raptor genomes identified common molecular signatures that underpin anatomical structure and sensory, muscle, circulatory, and respiratory systems related to a predatory lifestyle. Compared with diurnal birds, owls exhibit striking adaptations to the nocturnal environment, including functional trade-offs in the sensory systems (e.g., loss of color vision genes and selection for enhancement of nocturnal vision and other sensory systems) that are probably convergent with other nocturnal avian orders. Additionally, we found that a suite of genes associated with vision and circadian rhythm were differentially expressed between nocturnal and diurnal raptors, indicating adaptive expression change during the transition to nocturnality.\n\nConclusionsOverall, raptor genomes showed genomic signatures associated with the origin and maintenance of several specialized physiological and morphological features essential to be apex predators.

genomics↗

bioRxiv2018

Cognitive functions and jugular venous reflux in severe mitral regurgitation

Cardiac diseases with elevated central venous pressure have higher frequency of jugular venous reflux (JVR), which is associated with decreased cerebral blood flow and white matter hyperintensities. Whether patients with severe mitral-regurgitation (SMR) have poorer cognitive functions and whether JVR is involved were determined. Patients with SMR and age/sex-matched controls were prospectively recruited. Neuropsychological tests such as global cognitive (Mini-Mental State Examination, MMSE), verbal memory, executive, and visuospatial domains were performed. Cardiac parameters by cardiac catheterisation and echocardiography, and the frequency of JVR by colour-coded duplex ultrasonography were obtained. Forty patients with SMR and 40 controls (71.1{+/-}12.2, 38-89 years; 75% men) were included. Compared with the controls, patients with SMR had lower scores in all neuropsychological tests but only MMSE and visuospatial test scores were statistically significant after adjusting for age, sex, and educational level. We further adjusted for cardiovascular risk factors; the significance remained in the visuospatial test but diminished in MMSE. Multivariate linear regression analyses adjusted for age, sex, and educational level showed that JVR combined with high right-atrial-pressure (RAP > 50th-percentile, 12 mmHg) was significantly associated with poorer performances in both MMSE [right JVR: B coefficient(95% confidence interval, p)=-2.83(-5.46-0.20, 0.036); left JVR: -2.77(-5.52-0.02, 0.048)] and visuospatial test [right JVR: -4.52(-8.89-0.16, 0.043); left JVR: -4.56(-8.81-0.30, 0.037)], with significances that remained after further adjusting for cardiovascular risk factors. Our results suggest that retrogradely-transmitted venous pressure might be involved in the mechanisms mediating the relationship between cardiac diseases and brain functions.

neuroscience↗

bioRxiv2017

Multiple reference genome sequences of hot pepper reveal the massive evolution of plant disease resistance genes by retroduplication

Transposable elements (TEs) provide major evolutionary forces leading to new genome structure and species diversification. However, the role of TEs in the expansion of disease resistance gene families has been unexplored in plants. Here, we report high-quality de novo genomes for two peppers (Capsicum baccatum and C. chinense) and an improved reference genome (C. annuum). Dynamic genome rearrangements involving translocations among chromosome 3, 5 and 9 were detected in comparison between C. baccatum and the two other peppers. The amplification of athila LTR-retrotransposons, members of the gypsy superfamily, led to genome expansion in C. baccatum. In-depth genome-wide comparison of genes and repeats unveiled that the copy numbers of NLRs were greatly increased by LTR-retrotransposon-mediated retroduplication. Moreover, retroduplicated NLRs exhibited great abundance across the angiosperms, with most cases lineage-specific and thus recent events. Our study revealed that retroduplication has played key roles in the emergence of new disease-resistance genes in plants.

plant biology↗