Biology subjects

Deb, S.

Publications and source records attributed to Deb, S..

At least 19 recordsLinked to original sources

bioRxiv2026

Modulation of the speed of Intrinsic Alpha Frequency (IAF) with tACS modulates variability of illusory speech perception

Navigating the world requires our brains to constantly process a massive influx of information from the environment. One of the most remarkable yet complex feats the human brain performs daily is speech perception. It is a multifaceted, hierarchical process that relies heavily on the integration of auditory and visual cues, particularly in noisy environments. Neural integration of these streams is hypothesized to depend on temporal mechanisms governed by individual alpha frequency (IAF, 8-12 Hz), which serves as a key neural correlate of the temporal binding window (TBW). While IAF has been linked to multisensory integration, its role in shaping multisensory illusions remains largely unexplored. Here, we tested this directly using transcranial alternating current stimulation (tACS) to modulate occipital activity during multisensory conflict. In a two-day protocol involving 27 healthy participants, resting-state EEG was recorded to determine IAF. On Day 2, participants then performed a multisensory speech task involving congruent (pa/, /ta/, /ka/) and incongruent McGurk stimuli (auditory /pa/, visual /ka/), both at baseline and during tACS applied at IAF and offset frequencies (IAF +/- 2 Hz) over occipital electrodes. While accuracy for congruent syllables remained high across conditions, results revealed that tACS significantly reduced the perception of illusory /ta/ percepts during McGurk trials. Finally, using a phenomenological model based on Kuramoto oscillators, we provided a mechanistic explanation for the percentage of illusory responses observed across participants under the influence of tACS at IAF and offsets. This study highlights the potential for targeted neuromodulatory interventions to influence multisensory processing in clinical or professional settings.

neuroscience↗

bioRxiv2026

Reciprocal feedback inhibition and divergent intrinsic firing properties between behaviorally defined classes of neurons in the mouse ventromedial hypothalamus

The capacity to orchestrate appropriate defensive behaviors in response to threatening stimuli is essential for the survival of organisms. Flight, freezing, appeasement, and attack, for example, are common defensive responses evoked depending upon the nature of the threat, the immediate context, and past experiences. Multiple brain regions have been implicated in regulating such responses, with the medial hypothalamus playing a key role in mediating innate responses to social and predator threats. The ventrolateral subdivision of the ventromedial hypothalamus (VMHvl) has been shown to mediate both avoidance and aggression towards conspecific threats in mice, suggesting that it serves as a circuit for context-appropriate defensive responses to social threats. Previous in vivo calcium imaging in VMHvl identified cells whose activity encodes either approach toward or escape from a social threat (Assessment+ and Flight+ cells, respectively), but it remained unclear how the switch in neural encoding from approach to avoidance occurs. Here, we use in vivo single-unit electrophysiology recordings coupled to channelrhodopsin-assisted circuit mapping (optrodes) to explore the functional and structural connectivity basis of the approach-avoidance switch. We confirm the presence of Assessment+ and Flight+ neurons in VMHvl and demonstrate that they are interconnected through feedback excitation and reciprocal feedback inhibition. Moreover, we discover that Assessment+ and Flight+ neurons exhibit a pronounced difference in their intrinsic firing properties. We hypothesize that this asymmetry in intrinsic responsivity coupled to reciprocal feedback inhibition underlies the nonlinear firing changes at the approach-to-avoidance transition and plays a role in triggering escape behavior.

neuroscience↗

bioRxiv2026

Powdery mildew fungi block plant vacuolar traffic to suppress immunity

Plant immunity can be activated by membrane-localized pattern recognition receptors or by cytosolic nucleotide-binding leucine-rich repeat (NLR) receptors, while it can be counteracted by pathogen secreted effectors. Manifestation of immunity often involves endomembrane traffic. However, limited evidence is available for such an involvement in NLR-mediated immunity, which typically includes a hypersensitive reaction (HR)-programmed cell death response. Here we show that the barley powdery mildew fungus uses several effectors to target and inhibit the vacuolar trafficking pathway, which causes endomembrane markers to stall in the endoplasmic reticulum (ER). We used this ER-stalling phenotype as a proxy to track fungal manipulation of the vacuolar pathway during different stages of the actual infection. Our data indicate that powdery mildew fungi interfere with the vacuolar pathway, but only temporarily, as the stalling is lifted once the fungal haustorial feeding structures are well-developed for nutrient uptake in epidermal cells. Notably, we show evidence that blocking the vacuolar pathway causes a general inhibition of NLR-mediated HR, and that this mechanism is taken advantage of by the pathogen. Finally, we provide an example that the fungus can secrete a different set of effectors at the haustorial stage that result in the re-opening of the vacuolar pathway by inhibiting the initial vacuolar traffic-suppressing effectors.

plant biology↗

bioRxiv2025

MosaicSim: A Novel Mosaic Variant Simulator Reveals Diminishing Returns of Ultra-High Coverage for Mosaic Variant Detection

Genetic mutations within select cells of a tissue, termed mosaic variants (MV), are being increasingly recognized for their role in human disease. This growing interest underscores the need for specialized tools to detect and analyze MVs. However, such detection methods still lack thorough evaluation, largely due to missing benchmarking datasets that are large, reliable, and reflective of the complexity of biological samples. To address this gap, we developed MosaicSim, a tool for simulating variants in realistic sequencing data. The TweakVar workflow is at the tools core and represents a unique simulation pipeline that layers simulated MVs onto empirical whole genome sequencing data, generating a large, realistic ground truth dataset that combines the strengths of both simulation and biological data. To demonstrate the functionality of the workflow, we simulated 1,000 mosaic single nucleotide polymorphisms using TweakVar within whole genome sequencing files of different coverages. MVs were called with Illuminas DRAGEN and compared to the ground truth. Our results show 150x-445x coverage performed comparably, with a true-positive rate between 50.4% (300x) and 54.9% (150x) and no false-positives detected. Across all samples, increasing variant allele frequency had a significant positive effect on call success. Additionally, we observed that call rates for variants in lower complexity regions improved with increasing read depth. We did not find significant effects attributable to specific mutation patterns or mean read map quality. MosaicSim fills a critical unmet need by providing representative, customizable ground truth datasets for MV benchmarking, enabling systematic evaluation and optimization of variant calling methods.

genomics↗

bioRxiv2025

Immediate early genes act in the medial hypothalamus to promote adaptation to social defeat

Territorial animals must moderate their social aggression and avoidance behaviors in a manner that maximizes their access to resources and fitness. The ventrolateral division of the ventromedial hypothalamic nucleus (VMHvl) has been shown to control both social aggression and avoidance in mice, and emerging data show that neural plasticity within VMHvl can drive the experience-dependent adaptation of these behaviors. Here, we investigated the contribution of immediate early gene (IEG) function in supporting this plasticity. In initial experiments, we found that downregulation of the IEG cFos in VMHvl did not significantly moderate the long-term increase in social avoidance seen following an experience of social defeat. However, local knockout of the IEG master regulator Serum Response Factor (SRF, Srf) was able to blunt the impact of social defeat on social avoidance and prevented the effect of social defeat on local optogenetic-evoked social avoidance behavior, demonstrating a critical role for subcortical IEG activity in social defeat-induced behavioral plasticity. To test whether NMDA receptor dependent plasticity might be involved in this effect, we locally infused the NMDA receptor antagonist MK-801 into VMHvl and assessed the impact of social defeat. Unexpectedly, MK-801 treatment led to an increase in social defeat-induced avoidance, pointing to the existence of opposing IEG and NMDA receptor-dependent adaptive mechanisms in medial hypothalamus. These findings suggest that multiple neural plasticity mechanisms are likely to be at play in the hypothalamic nuclei supporting innate behavior adaptation and show how IEG blockade can be used as a genetic tool to systematically map neural plasticity in the brain. Significance StatementThe role of IEGs in experience-dependent plasticity has not been investigated in subcortical structures until now. Our findings suggest IEGs expression is essential for adaptive behavioral changes in the VMHvl following social defeat and can potentially be used to map behavioral adaptation across brain regions. Our study also indicates a potential use of IEGs as targets of gene therapy for mitigating maladaptive behavioral adaptations.

neuroscience↗

bioRxiv2025

Green-Synthesized Silver Nanoparticles from Coconut: A Novel Antimicrobial Strategy Against Acne Pathogens

Acne vulgaris is a widespread dermatological disorder, often complicated by multidrug-resistant (MDR) bacteria such as Staphylococcus aureus. Rising resistance to conventional antibiotics has created an urgent need for alternative antimicrobial strategies. Nanoparticles, due to their nanoscale dimensions and unique surface properties, have shown considerable promise in overcoming bacterial resistance mechanisms. In this study, acne-associated bacteria were isolated and identified through biochemical and microscopic methods, followed by antibiotic susceptibility testing. The isolates exhibited resistance to commonly prescribed antibiotics including vancomycin, erythromycin, ampicillin, and amoxicillin. To address this, silver nanoparticles (AgNPs) were synthesized using coconut shell extract (CSE), a waste-derived, phenolic-rich material that acted both as a reducing and stabilizing agent in the green synthesis process. CSE-AgNPs demonstrated strong antibacterial activity against MDR S. aureus, producing clear zones of inhibition, reduced MIC values, and structural damage to bacterial cell walls. These findings highlight CSE-AgNPs as an eco-friendly, cost-effective, and potent antimicrobial alternative, integrating waste valorization with nanotechnology to combat antibiotic resistance in acne-associated pathogens.

microbiology↗

bioRxiv2025

Loss of intestinal endosome associated protein sorting nexin 27 disrupts epithelial barrier and promotes inflammation

Backgrounds and aimsSNX27, member of the sorting nexin (SNX) family, carries a unique PDZ domain and mediates recycling of endocytosed transmembrane proteins. SNX27 is critical for neurodevelopmental processes, however its role in intestine remains unexplored. We aim to determine the previously unknown roles of SNX27 in regulating intestinal homeostasis, epithelial barrier integrity, and inflammatory responses. MethodsWe used available datasets to analyze SNX27 expression in human IBD. We generated a novel mouse model of SNX27 conditional deletion from intestinal epithelial cells (SNX27{Delta}IEC) and challenged these mice with Dextran Sulfate Sodium (DSS). ResultsSNX27 expression was significantly lower in human IBD, including UC and CD. SNX27{Delta}IEC mice had significantly lower bodyweight and exhibited increased proliferation and poor differentiation of secretory Paneth and Goblet cells. We found reduced mucin layer and downregulation of crucial epithelial barrier proteins {Delta}-catenin, E-cadherin, ZO-1, and Claudin10 in SNX27{Delta}IEC mice. SNX27{Delta}IEC mice showed high intestinal permeability and spontaneously developed intestinal inflammation. Moreover, SNX27{Delta}IEC mice were more susceptible towards DSS-induced colitis, compared to the SNX27Loxp mice. ConclusionOverall, deletion of intestinal epithelial SNX27 weakens barrier functions and promotes inflammation. Our results indicate a novel role of SNX27 in regulating intestinal physiology and protecting against intestinal disorders. Thus, understanding the mechanisms of SNX27 downregulation in IBD will provide insights into new prevention and targets against chronic inflammation. SynopsisO_LISNX27 recycles internalized transmembrane proteins in the endocytic pathway. Human IBD showed reduced levels of SNX27. C_LIO_LISNX27 plays novel functions by maintaining intestinal homeostasis and inhibiting inflammation. C_LIO_LISNX27 protects the host against losing intestinal integrity during inflammation. C_LI

physiology↗

bioRxiv2024

Amyloid signaling in antiphage defense

Immune regulated cell death (RCD) is a defense strategy common to different domains of life involving purposeful sacrifice of infected cells. In animals and fungi, functional amyloids play a role in the control of RCD as molecular switches activating key cell death effectors, rather than causing direct toxicity as seen with pathological amyloids. Here, we describe a novel amyloid-based signal transduction mechanism in an antiphage defense system in Escherichia coli. This antiphage abortive infection (Abi) system is mediated by two proteins, Bab and Agp which share a common amyloid motif and are encoded by adjacent genes. Upon phage infection, Agp activates Bab through amyloid signaling, leading to cell death. We determined the structure of the Bab cell death execution domain, which is distantly related to pore-forming domains present in fungi, animals and plants. We show that Bab and the fungal HET-S amyloid-controlled cell death execution protein are functionally interchangeable in their respective roles in antiphage defense and allorecognition. These findings add antiphage defense to the functional repertoire of amyloids.

microbiology↗

bioRxiv2024

A powdery mildew core effector protein targets host endosome tethering complexes HOPS and CORVET

Powdery mildew fungi are serious pathogens of many plant species. Their genomes encode extensive repertoires of secreted effector proteins that suppress host immunity. Here, we revised and analyzed the candidate secreted effector protein (CSEP) effectome of the barley powdery mildew fungus, Blumeria hordei (Bh) and identified seven CSEPs that are broadly conserved in powdery mildew fungal species, rendering them core effectors of these phytopathogens. We show that one of these, CSEP0214, interacts with the barley VPS18 protein, a core component of the CORVET and HOPS endosomal tethering complexes, mediating fusions of early endosomes and multivesicular bodies with the central vacuole, respectively. Overexpression of CSEP0214 and knockdown of either VPS18, HOPS-specific VPS41 or CORVET-specific VPS8 caused a block of the vacuolar pathway and the accumulation of the fluorescent vacuolar marker protein (SP)-RFP-AFVY in the endoplasmic reticulum. Co-immunoprecipitation and yeast two-hybrid experiments suggest that CSEP0214 blocks the interaction of VPS18 and VPS16, which are both core components of CORVET as well as HOPS. Additionally, expression of CSEP0214 blocked the hypersensitive cell death response associated with resistance gene-mediated immunity in barley, indicating that endomembrane traffic is required for this process. It also prevented callose deposition in cell wall appositions at attack sites and encasements of fungal infection structures. Our results indicate that this powdery mildew core effector is an essential immunity suppressor. One sentence summaryThe Blumeria hordei effector protein CSEP0214 interacts with barley VPS18, a core component of the CORVET and HOPS endosomal tethering complexes, thereby interfering with host endomembrane trafficking.

plant biology↗

bioRxiv2024

Xanthomonas oryzae pv. oryzae type-III effector TAL9b targets a broadly conserved disease susceptibility locus to promote pathogenesis in rice

Xanthomonas oryzae pv. oryzae (Xoo), the causal agent of bacterial blight of rice, translocates multiple Transcription Activator-Like Effectors (TALEs) into rice cells. The TALEs localize to the host cell nucleus, where they bind to the DNA in a sequence-specific manner and enhance gene expression to promote disease susceptibility. Xoo strain PXO99A encodes nineteen TALEs, but the host targets of all these TALEs have not been defined. A meta-analysis of rice transcriptome profiles revealed a gene annotated as flavonol synthase/flavanone-3 hydroxylase (henceforth OsS5H/FNS-03g) to be highly induced upon Xoo infection. Further analyses revealed that this gene is induced by PXO99A using TAL9b, a broadly conserved TALE of Xoo. Disruption of tal9b rendered PXO99A less virulent. OsS5H/FNS-03g functionally complemented its Arabidopsis homologue AtDMR6, a well-studied disease susceptibility locus. Biochemical analyses suggested that OsS5H/FNS-03g is a bifunctional protein with Salicylic Acid 5 Hydroxylase (S5H) and Flavone Synthase-I (FNS-I) activities. Further, an exogenous application of apigenin on rice leaves, the flavone that is enzymatically produced by OsS5H/FNS-03g, promoted virulence of PXO99A tal9b-. Overall, our study suggests that OsS5H/FNS-03g is a bifunctional enzyme and its product apigenin is potentially involved in promoting Xoo virulence.

plant biology↗

bioRxiv2024

Oncogenic Mutant p53 Sensitizes Non-Small Cell Lung Cancer Cells to Proteasome Inhibition via Oxidative Stress-Dependent Induction of Mitochondrial Apoptosis

Non-small cell lung cancer (NSCLC) cells with oncogenic mutant p53 alleles (Onc-p53) exhibit significantly higher levels of proteasome activity, indicating that Onc-p53 induces proteotoxic stress which may be leveraged as a therapeutic vulnerability. Proteasome inhibitors (PIs), such as bortezomib (BTZ), can induce toxic levels of oxidative stress in cancer cells and thus we investigated whether PIs exhibit preferential cytotoxicity in Onc-p53 NSCLC cells. Indeed, BTZ and other PIs exhibited the IC50 6-7-fold lower in Onc-p53 cells vs. wild-type (WT) p53 cells. BTZ cytotoxic effects in Onc-p53 cells were nearly completely rescued by antioxidants such as N-acetyl cysteine, indicating that oxidative stress is the critical driver of BTZ-dependent cytotoxic effects in Onc-p53 cells. Importantly, we observed oxidative stress-dependent transcriptional induction of the pro-apoptotic NOXA with downstream cleaved caspase-3, consistent with apoptotic cell death in Onc-p53 but not in WT p53 cells treated with BTZ, and BTZ-generated oxidative stress was linked to nuclear translocation of NRF2 and transcriptional activation of ATF3, which in turn was required for NOXA induction. Validating BTZs translational potential in Onc-p53 NSCLC, BTZ and carboplatin or the BH3-mimetic navitoclax were synergistically cytotoxic in Onc-p53 but not WT p53 cells in vitro, and BTZ effectively limited growth of Onc-p53 NSCLC xenografts when combined with either carboplatin or navitoclax in vivo. Our data therefore support further investigation of the therapeutic utility of PIs combined with carboplatin or BH3-mimetics in Onc-p53 human NSCLC as novel therapeutic strategies. SignificanceNon-small cell lung cancer (NSCLC) is the leading cause of cancer death due, in part, to a lack of active therapies in advanced disease. We demonstrate that proteasome inhibitor/BH3-mimetic combination therapy is an active precision therapy in NSCLC cells and tumors expressing oncogenic mutant p53 alleles (Onc-p53).

cancer biology↗

bioRxiv2024

Efficacy of dynamic eigenvalue in anticipating and distinguishing tipping points

The presence of tipping points in several natural systems necessitates having improved early warning indicators to provide accurate signals of an impending transition to a contrasting state while also detecting the type of transition. Various early warning signals (EWSs) have been devised to forecast the occurrence of tipping points, also called critical transitions. Dynamic eigenvalue (DEV) is a recently proposed EWS that can not only predict the occurrence of a transition but also certain types of accompanying bifurcations. Here, we study the effectiveness and limitations of DEV as an EWS for diverse kinds of critical phenomena. We demonstrate that DEV is a powerful EWS that shows promising results in anticipating catastrophic (first-order or discontinuous) and non-catastrophic (second-order or continuous) transitions in discrete and continuous dynamical systems. However, it falls short in the case of piecewise smooth systems. Further, the ability of DEV to forecast the type of transition is limited, as it cannot differentiate saddle-node bifurcation from transcritical and pitchfork bifurcations. Despite these limitations, we show that DEV can work as a robust indicator for varying rates at which the transition is approached and with systems involving colored noise.

ecology↗

bioRxiv2023

Early warning signals are hampered by a lack of critical transitions in empirical lake data

Quantifying the potential for abrupt non-linear changes in ecological communities is a key managerial goal, leading to a significant body of research aimed at identifying indicators of approaching regime shifts. Most of this work has built on the theory of bifurcations, with the assumption that critical transitions are a common feature of complex ecological systems. This has led to the development of a suite of often inaccurate early warning signals (EWSs), with more recent techniques seeking to overcome their limitations by analysing multivariate time series or applying machine learning. However, it remains unclear whether regime shifts and/or critical transitions are common occurrences in natural systems, and - if they are present - whether classic and second-generation EWS methods predict rapid community change. Here, using multitrophic data on nine lakes from around the world, we both identify the type of transition a lake is exhibiting, and the reliability of classic and second generation EWSs methods to predict whole ecosystem change. We find few instances of critical transitions in our lake dataset, with different trophic levels often expressing different forms of abrupt change. The ability to predict this change is highly technique dependant, with multivariate EWSs generally classifying correctly, classical rolling window univariate EWSs performing not better than chance, and recently developed machine learning techniques performing poorly. Our results suggest that predictive ecology should start to move away from the concept of critical transitions and develop methods suitable for predicting change in the absence of the strict bounds of bifurcation theory.

ecology↗

bioRxiv2022

Tipping points in spatial ecosystems driven by correlated noise

Complex spatial systems can experience critical transitions or tippings on crossing a threshold value in their response to stochastic perturbations. Whilst previous studies have well-characterized the impact of white noise on tipping, the effect of correlated noise in spatial ecosystems remains largely unexplored. Here, we investigate the effect of both multiplicative and additive Ornstein-Uhlenbeck (OU) correlated noise on the occurrence of critical transitions in spatial ecosystems. We find that decreasing the noise correlation aggravates the chance of critical transitions - opposite to what is observed previously in temporal systems in the presence of OU-noise with fixed lag-1 correlation. Our results hold good and are supported by the analysis of three well-studied spatial ecological models of varying nonlinearity. We also compute spatial early warning indicators (e.g., spatial variance, spatial skewness, and spatial correlation) to determine their reliability in anticipating tipping points with variations in noise correlation. The indicators of critical transitions exhibit mixed success in forewarning the occurrence of a tipping point, as indicated by the distribution of Kendalls rank correlation.

ecology↗

bioRxiv2022

Extraintestinal roles of intestinal vitamin D receptor in protecting against dysbiosis and tumorigenesis in breast cancer

The microbiota play critical roles in regulating the function and health of intestine and extraintestinal organs. A fundamental question is whether there is an intestinal-microbiome-breast axis during the development of breast cancer. If yes, what are the roles of host factors? Vitamin D receptor (VDR) involves host factors and the human microbiome. Vdr gene variation shapes the human microbiome and VDR deficiency leads to dysbiosis. We hypothesized that intestinal VDR protects hosts against tumorigenesis in breast. Reduced VDR mRNA expression was observed in patients with breast cancer. We used a 7,12-dimethylbenzanthracene (DMBA)-induced breast cancer model in intestinal epithelial VDR knockout (VDR{Delta}IEC) mice. We reported that VDR{Delta}IEC mice with dysbiosis are more susceptible to breast cancer induced by DMBA. Intestinal and breast microbiota analysis showed that lacking VDR leads to bacterial profile shift from normal to susceptible carcinogenesis. We found enhanced bacterial staining within breast tumors. At the molecular and cellular levels, we identified the mechanisms by which intestinal epithelial VDR deficiency led to increased gut permeability, disrupted tight junctions, microbial translocation, and enhanced inflammation, thus increasing the tumor size and number in breast. Furthermore, treatment with beneficial bacterial metabolite butyrate or probiotic Lactobacillus plantarum reduced the breast tumors, enhanced the tight junctions, and inhibited inflammation in the VDR{Delta}IEC mice. Gut microbiome contribute to the pathogenesis of diseases, not only in the intestine, but also in the breast. Our study provides new insights into the mechanism by which intestinal VDR dysfunction and gut dysbiosis led to high risk of extraintestinal tumorigenesis. Gut-tumor-microbiome interactions indicate a new target in the prevention and treatment of breast cancer. O_FIG O_LINKSMALLFIG WIDTH=165 HEIGHT=200 SRC="FIGDIR/small/492300v1_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@7e354eorg.highwire.dtl.DTLVardef@1dd9b50org.highwire.dtl.DTLVardef@1ffe2c5org.highwire.dtl.DTLVardef@810b1a_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

bioRxiv2022

SARS-CoV-2 Omicron Variant Wave in India: Advent, Phylogeny and Evolution

SARS-CoV-2 evolution has continued to generate variants, responsible for new pandemic waves locally and globally. Varying disease presentation and severity has been ascribed to inherent variant characteristics and vaccine immunity. This study analyzed genomic data from 305 whole genome sequences from SARS-CoV-2 patients before and through the third wave in India. Delta variant was responsible for disease in patients without comorbidity(97%), while Omicron BA.2 caused disease primarily in those with comorbidity(77%). Tissue adaptation studies brought forth higher propensity of Omicron variants to bronchial tissue than lung, contrary to observation in Delta variants from Delhi. Study of codon usage pattern distinguished the prevalent variants, clustering them separately, Omicron BA.2 isolated in February grouped away from December strains, and all BA.2 after December acquired a new mutation S959P in ORF1b (44.3% of BA.2 in the study) indicating ongoing evolution. Loss of critical spike mutations in Omicron BA.2 and gain of immune evasion mutations including G142D, reported in Delta but absent in BA.1, and S371F instead of S371L in BA.1 could possibly be due to evolutionary trade-off and explain very brief period of BA.1 in December 2021, followed by complete replacement by BA.2.

genomics↗

bioRxiv2022

Rising Temperature Drives Tipping Points in Mutualistic Networks

The effect of climate warming on species physiological parameters, including growth rate, mortality rate, and handling time, is well established from empirical data. However, with an alarming rise in global temperature more than ever, predicting the interactive influence of these changes on mutualistic communities remains uncertain. Using 139 real plant-pollinator networks sampled across the globe and a modelling approach, we study the impact of species individual thermal responses on mutualistic communities. We show that at low mutualistic strength plant-pollinator networks are at potential risk of rapid transitions at higher temperatures. Evidently, generalist species plays a critical role in guiding tipping points in mutualistic networks. Further, we derive stability criteria for the networks in a range of temperatures using a two-dimensional reduced model. We identify network structures that can ascertain the delay of a community collapse. Until the end of this century, many real mutualistic networks can be under the threat of sudden collapse, and we frame strategies to mitigate them. Together, our results indicate that knowing individual species thermal responses and network structure can improve predictions for communities facing rapid transitions.

ecology↗

bioRxiv2022

Pan-genome evolution and its association with divergence of metabolic functions in Bifidobacterium genus

Many works have been performed to characterize the genomic evolution and diversity among type species of the Bifidobacterium genus due to its health-promoting effect on their host. However, those studies were mainly based on species-level taxonomic resolution, adaptation, and characterization of carbohydrate metabolic features of the bifidobacterial species. Here, a comprehensive analysis of the type strain genome unveils the association of pan-genome evolution with the divergence of metabolic function of the Bifidobacterium genus. This study also has demonstrated that the horizontal gene transfer and genome expansion and reduction events in the evolutionary history influencing the diversity of metabolic functions of bifidobacterium genus. Furthermore, the genome-based search of probiotic traits among all the available bifidobacterial type strains gives hints on type species, that could confer health benefits to nutrient-deficient individuals. Altogether, the present study provides insight into the developments of genomic evolution, functional divergence, and potential probiotic type species of the Bifidobacterium genus.

genomics↗