Biology subjects

Kaur, T.

Publications and source records attributed to Kaur, T..

At least 19 recordsLinked to original sources

bioRxiv2026

Gut-Associated Metabolites (GAMs) revitalize dysfunctional CD8⁺ T lymphocytes in Osteosarcoma

Osteosarcoma (OS) is one of the top ranking and deadliest primary malignant bone tumor of youngsters and adolescents. OS has poor prognostic features due to its immunosuppressive "cold" tumor microenvironment, obstructing the anti-tumor effector functions of immune cells (including cytotoxic CD8 T lymphocytes). Recent developments have focused on the role of Gut Microbiota in modulating effector immune responses in various cancers. However, the immunomodulatory role of gut microbiota and its derived gut-associated metabolites (GAMs) in OS still remains unclear. Here we report that peripheral CD8 T lymphocytes in osteosarcoma patients are less frequent in circulation, hypo-producers of effector cytokines (IFN-{gamma} and TNF-), and have compromised metabolic fitness. We characterized and investigated the effect of a panel of microbiota-derived GAMs on CD8 T lymphocytes, confirming their immunomodulatory role with respect to CD8 T lymphocytes activation, cellular metabolism and effector functions. Indole-3-lactic acid (ILA; product of tryptophan metabolism), was observed to be the strongest immunostimulant among all the GAMs studied. ILA enhanced the anti-tumor effector functions of CD8 T lymphocytes through increased glucose uptake, a higher mitochondrial bio-mass and increased production of IFN-{gamma} and TNF-. Moreover, ILA-primed cytotoxic T lymphocytes exhibited considerably higher cytotoxicity and increased apoptosis of osteosarcoma cells (U2OS). Altogether, our data demonstrates that ILA acts as a microbial-derived immune modulator to metabolically reprogram and restore dysfunctional CD8 T lymphocytes against osteosarcoma. This study for the first time demonstrates the therapeutic potential of exploiting the nexus between "Gut-Immune-Bone Tumor" ternary as a safe and cost-effective combinatorial immunotherapy against osteosarcoma. Graphical AbstractIndole-3-Lactic Acid (ILA) Reinvigorates CD8+ T-Cell Immunity in Osteosarcoma Circulating CD8+ T cells from osteosarcoma patients exhibit impaired metabolic fitness, reduced effector cytokine production, and diminished tumoricidal activity. Screening of gut-associated metabolites identified the microbial tryptophan metabolite indole-3-lactic acid (ILA) as the most potent immunomodulator. ILA restores glucose uptake and mitochondrial biomass, enhances IFN-{gamma} and TNF- production, promotes polyfunctional CD8+ T-cell responses, and significantly improves CTL-mediated killing of osteosarcoma cells, highlighting its potential as a microbiota-derived immunometabolic therapeutic for osteosarcoma. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=113 SRC="FIGDIR/small/741694v1_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@19809aforg.highwire.dtl.DTLVardef@a3eb09org.highwire.dtl.DTLVardef@19bada3org.highwire.dtl.DTLVardef@1a4c4da_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

bioRxiv2026

Resting State Somatomotor Functional Brain Networks using Empirical Mode Decomposition and Hilbert Transformation

The goal of the resting-state functional connectivity studies is to determine the inherent dynamics of the brain networks while the body is at rest. These networks get differentially activated when the brain is involved in various tasks such as processing of sensory inputs, initiating motor activities, or various cognitive tasks. Resting state functional connectivity networks are commonly revealed by determining Pearson Correlation Coefficients of the Blood Oxygenation Level Dependent (BOLD) signals collected from different brain regions using functional Magnetic Resonance Imaging (fMRI) while the subject is not actively performing any task. However, the functional connectivity thus determined does not correlate well with the known structural connectivity between different brain regions. Here, we used Empirical Mode decomposition (EMD), followed by Hilbert Transformation (HT), to determine the resting state functional connectivity in the human brains. We show the advantage of using this EMD-HT method using somatomotor network as an example. We show that the time series data decomposed by this method improves correlation of the derived functional connectivity with the known structural connectivity (especially for low -TR fMRI data) as compared to the methods commonly used.

neuroscience↗

bioRxiv2025

Failure of DNA repair leads to the tumorigenic transformation of a regenerating blastema in Drosophila imaginal discs

We present a Drosophila model demonstrating that repeated cycles of tissue regeneration following localized apoptosis can induce tumorigenesis in the absence of oncogene activation or tumor suppressor loss. Chronic regenerative stress leads to epithelial disorganization, loss of cell polarity, immune cell infiltration, DNA damage, centrosomal defects, and aneuploidy-- classical hallmarks of cancer. A subset of "walking dead" cells resists apoptosis and contributes to tissue overgrowth and heterogeneity. Single-cell transcriptomics identifies a distinct cell population, absent from normal tissue, emerging under both regenerative and tumorigenic conditions and characterized by enrichment in JNK pathway components. The tumorigenic signature specifically features distinctive JNK regulatory elements while excluding chaperone proteins. Notably, inhibition of JNK signaling or modulation of DNA repair suppresses neoplastic transformation. This model reveals how chronic injury and defective regeneration drive cancer initiation, establishing a mechanistic link between wound healing and tumorigenesis, and providing a powerful system to explore early tumor development and therapeutic intervention.

developmental biology↗

bioRxiv2025

CX3CR1 Fate-Mapping In Vivo Distinguishes Cochlear Resident and Recruited Macrophages After Acoustic Trauma

Cochlear injury activates the resident macrophages (RM) and recruits the blood-circulating monocytes and monocyte-derived macrophages (Mo/Mo-M), but their specific functions in the injured cochlea are unknown. It is well established that the chemokine fractalkine receptor (CX3CR1), expressed by cochlear macrophages, influences the density of those macrophages and promotes synaptic repair and spiral ganglion neuron survival in the injured cochlea. As CX3CR1 is expressed on both RM and Mo/Mo-M, it remains unclear if CX3CR1-expressing RM and Mo/Mo-M are distinct and differentially promote SGN survival after cochlear injury. Here, we demonstrate the use of fate mapping via a tamoxifen-inducible CX3CR1 mouse model (CX3CR1YFP-CreERT2/wildtype:R26RFP) wherein CX3CR1-expressing RM and Mo/Mo-M are endogenously labeled with different fluorescent reporters to define the heterogeneity in cochlear macrophages regarding their origin, turnover, spatiotemporal distribution, morphology, and fate following a loud acoustic trauma. After 60 days of tamoxifen injections at 4 weeks of age, long-lived cochlear RM were YFP+ RFP+ with 98.0 {+/-} 1.7% recombinant efficiency, and short-lived blood-circulating CX3CR1 lineage (Mo/Mo-M) were YFP+ RFP-with 2.5 {+/-} 1.1% recombinant efficiency. Following an acoustic trauma of 112 dB SPL at 8-16 kHz octave band for 2 hours, morphologically similar RM and Mo/Mo-M were observed in the spiral ganglion, lamina, ligament, and around the sensory epithelium. Quantification of RM and Mo/Mo-M in the spiral lamina and ganglion revealed distinct spatial and temporal distribution patterns. Furthermore, recruited Mo/Mo-M expressed classical monocyte markers such as Ly6C and CCR2. Both RM and Mo/Mo-M were positive for proliferation marker, Ki67, and negative for apoptotic marker, cleaved caspase-3, suggesting that the overall increase in macrophage numbers in the noise-injured cochlea is a contribution of both the proliferation of RM and recruitment of Mo/Mo-M. Probing for blood-clotting protein, fibrinogen, showed its presence in the cochlea after acoustic trauma, suggesting vascular damage that positively and strongly correlated with the time course of recruitment of blood-circulating Mo/Mo-M in the noise-injured cochlea. These data imply that macrophages in the noise-injured cochlea are heterogeneous regarding their ontogeny, distribution, and fate. They offer a robust tool to study the precise roles of resident and recruited macrophages in healthy and pathological ears. SummaryUsing the novel CX3CR1 fate-mapping model, our data uncover diversity of macrophages with respect to their ontogeny, turnover, spatiotemporal distribution, and fate in the normal and noise-injured cochlea.

cell biology↗

bioRxiv2025

Variation in inbreeding depression within and among Caenorhabditis species

Outbreeding populations harbor large numbers of recessive deleterious alleles that reduce the fitness of inbred individuals, and this inbreeding depression potentially shapes the evolution of mating systems, acting as a counterweight to the inherent selective advantage of self-fertilization. The population biological factors that influence inbreeding depression are numerous and often difficult to disentangle. We investigated the utility of obligately-outcrossing (gonochoristic) Caenorhabditis nematodes as models for inbreeding depression. By systematically inbreeding lines from ten populations and tracking line extinction, we found that inbreeding depression is universal but highly variable among species and populations. Inbreeding depression was detected across the life cycle, from mating to embryo production to embryonic viability and larval growth, and reciprocal crosses implicated female-biased effects. In most cases, the surviving inbred lines have dramatically reduced fitness, but the variance among inbred lines is substantial and compatible with the idea that inbreeding depression need not be an obstacle to the evolution of selfing in these worms. Populations of some species, including Caenorhabditis becei, exhibited modest inbreeding depression and could be tractable laboratory models for gonochoristic Caenorhabditis.

evolutionary biology↗

bioRxiv2025

The equalizing effect of adaptive foraging increases plant coexistence in plant-pollinator networks

The role of pollination in plant coexistence remains contested, with studies using Lotka-Volterra models suggesting pollination hinders while consumer-resource approaches indicating it can promote plant coexistence. Through the lens of modern coexistence theory, we analyze how network nestedness and pollinator foraging behavior influence plant coexistence via stabilizing (increasing the relative effect of intraspecific to interspecific competition) or equalizing (reducing fitness differences) mechanisms. Our findings reveal that while nestedness alone threatens specialist plant persistence, adaptive foraging by pollinators generates equalizing mechanisms by benefiting specialist over generalist plants which promotes plant coexistence, helping explain the contrasting conclusions from previous studies.

ecology↗

bioRxiv2024

Knockdown-resistance (kdr) mutations in Indian Aedes aegypti populations: lack of recombination among haplotypes bearing V1016G, F1534C, and F1534L kdr alleles

BackgroundKnockdown resistance (kdr) mutations in the voltage-gated sodium channel (VGSC) gene are a key mechanism of insecticide resistance in mosquitoes. In Asian Aedes aegypti populations two main VGSC haplogroups with kdr mutations have been identified: one carrying the F1534C mutation and another with V1016G and/or S989P mutations. Functional studies have demonstrated that these three mutations on a single haplotype confer up to a 1100-fold increase in pyrethroid resistance, underscoring the need to monitor these triple mutations within distinct populations. This study investigates the prevalence of kdr mutations in Indian populations and explores the linkage association between these mutations and two distinct conserved types of introns located between exons 20 and 21. MethodsAe. aegypti specimens collected from eight different locations were genotyped for kdr alleles and intron (between exons 20 and 21) haplotypes using PCR-based assays. Representative samples underwent DNA sequencing of VGSC regions. ResultsFive kdr mutations namely S989P, V1016G, T1520I, F1534C, and F1534L, were identified, each exhibiting varying distribution and frequencies across different geographical regions. Two distinct and stably-diverged intron haplotypes, designated as intron-A and intron-B, were identified between exons 20 and 21. Seven haplotypes, including two wild-type variants, were observed among Indian populations. The kdr-bearing haplotypes can be classified into three distinct haplogroups: haplogroup G (V1016G with/or without S989P and with intron-A), haplogroup L (F1534L and intron-A), and haplogroup C (F1534C with/or without T1520I and with intron-B). Importantly, no evidence of recombination within Indian populations was detected among these three haplogroups. ConclusionsFive kdr mutations were identified in the VGSC of Indian Ae. aegypti populations, each showing a definitive linkage with one of the two types of intron haplotypes. The lack of recombination among haplogroups bearing 1016G with 989P, 1534C and 1534L mutations suggests that the most potent insecticide resistance haplotype, bearing the triple kdr mutation, is currently absent. This finding has significant operational implications, as it may indicate that current vector control measures remain effective against these populations, potentially delaying the emergence of highly resistant phenotypes

zoology↗

bioRxiv2024

Local Delivery of Soluble Fractalkine (CX3CL1) Peptide Restore Ribbon Synapses After Noise-Induced Cochlear Synaptopathy

Efficacy of chemokine fractalkine isoforms was evaluated for restoration of loss of inner hair cell ribbon synapses and hearing after noise-induced cochlear synaptopathy (NICS). Previously, we have demonstrated a critical role for fractalkine signaling axis (CX3CL1-CX3CR1) in synaptic repair where in the presence of fractalkine receptor (CX3CR1) expressed by cochlear macrophages, the damaged synapses are spontaneously repaired. Here, we examined whether overexpression of fractalkine ligand (CX3CL1 or FKN) in the form of a peptide is effective in restoring the lost synapses and hearing after NICS. Remarkably, single transtympanic (TT) injection of soluble isoform of FKN (sFKN) peptide at 1 day after synaptopathic noise trauma showed significant recovery of ABR thresholds, ABR peak I amplitudes and ribbon synapses in both FKN-wildtype and knockout mice when compared to mice injected with full length membrane-bound FKN peptide (mFKN). Mechanistically, sFKN peptide treatment increased macrophage numbers in the cochlea and in the absence of those macrophages, sFKN failed to restore loss of synapses and hearing after NICS. Furthermore, sFKN treatment attenuated cochlear inflammation after noise overexposure without altering the expression of CX3CR1. Finally, sFKN peptide was detectable inside the cochlea localized to the sensory epithelium for 24 hours after TT injection. These data provide a robust proof-of-principle that local delivery of an immune factor, sFKN is effective in restoring lost ribbon synapses and hearing after NICS in a macrophage-dependent manner and highlights the potential of sFKN as an immunotherapy for cochlear synaptopathy due to noise or aging. SummaryTranstympanic delivery of soluble FKN peptide is effective in restoring lost inner hair cell ribbon synapses and hearing after noise-induced cochlear synaptopathy in a macrophage-dependent manner.

neuroscience↗

bioRxiv2023

Role of maternal, fetal and placental histopathology factors in the pathogenesis of retinopathy of prematurity.

PurposeTo investigate if maternal, fetal and placental vascular and/or molecular changes predict the risk for retinopathy of prematurity in preterm infants. MethodologyThe postnatal and antenatal data and placental histopathological changes; H&E staining of placental sections and molecular findings; gene expression analysis by qRT-PCR and protein expression by IHC at the maternal-fetal interface were collected from 20 placental samples and categorized into 3 groups: full-term (n=10), preterm without ROP (n=7) and preterm with ROP (n=6). ResultsThe correlation analysis indicated significant association of increased monocytes (p=0.042), fetal growth retardation (p=0.000), apnoeic spell (p=0.033), ventilation (p=0.009), length in hospital stay (p=0.001) and decreased RBC (p=0.02), Hb (p=0.048), PCV (p=0.010), gestational age (p=0.003), birth weight (p=0.000) with increased risk of ROP. Along with these factors, placental weight(p=0.001), diameter (p=0.019), Tenny-Parker changes (p=0.025), alternating area of small and short hyper mature villi (p=0.033) are also found to be significant determinants of the disease. Gene expression analysis revealed significant increase in hypoxia (HIF-1 gene expression; p=0.007) and non-significant increase in the pro-inflammatory marker IL-6. The protein expression also showed the significantly increased activation of complement pathway (CFH) and NF- KB at maternal-fetal interface. ConclusionsOur preliminary results support the changes in the maternal-fetal factors, placental histopathology and molecular alterations related to hypoxia, inflammation and complement activation at maternal-fetal interface in preterm with ROP placentas. These changes have the potential to predict the risk of the disease but the results are required to be further validated in larger cohort.

pathology↗

bioRxiv2022

Molecular tools for early detection of invasion of malaria vector Anopheles stephensi

There are increasing reports of the expansion of the Asian malaria vector Anopheles stephensi in new geographical areas posing a threat to the elimination of urban malaria. Efficient surveillance of this vector in affected areas and early detection in new geographical areas is key for the containment and control of this species. To overcome the practical difficulties associated with the morphological identification of immature stages and adults of An. stephensi, a species-specific PCR and a Real-Time PCR assay were developed for their identification targeting a unique segment of ITS2 lacking homology to any other organism. Both PCRs can be used to identify An. stephensi individually or in pooled samples of mixed species, including when present in extremely low proportion. This study also reports a method for selective amplification and sequencing of An. stephensi for their confirmation in pooled samples of mixed species.

molecular biology↗

bioRxiv2022

Caenorhabditis nematodes colonize ephemeral resource patches in neotropical forests.

Factors shaping the distribution and abundance of species include life-history traits, population structure, and stochastic colonization-extinction dynamics. Field studies of model species groups help reveal the roles of these factors. Species of Caenorhabditis nematodes are highly divergent at the sequence level but exhibit highly conserved morphological uniformity, and many of these species live in sympatry on microbe-rich patches of rotten material. Here, we use field experiments and large-scale opportunistic collections to investigate species composition, abundance, and colonization efficiency of Caenorhabditis in two of the worlds best studied lowland tropical field sites: Barro Colorado Island in Panama and La Selva in Sarapiqui, Costa Rica. We observed seven species of Caenorhabditis, four of them known only from these collections. While these localities contain species from many parts of the phylogeny, both localities were dominated by globally distributed androdiecious species. We found that Caenorhabditis were able to colonize baits accessible only by phoresy, preferring to colonize baits making direct contact with the ground. We estimate founder numbers per colonization event to be low.

ecology↗

bioRxiv2021

Evaluation of odorant-binding protein-1 as a molecular marker for identifying biological forms and delimitating sibling species of Anopheles stephensi

BackgroundAnopheles stephensi, an invasive malaria vector, has been reported to have three biological forms identifiable mainly based on the number of ridges present on the eggs floats. Recently, the first intron of the odorant-binding protein-1 (AsteObp1) has been introduced as a molecular marker for the identification of these forms, and based on this marker, the presence of three putative sibling species (designated as species A, B and C) has been proposed. However, there is no data on the association of proposed markers with biological form or putative species on field populations. MethodsField collected and laboratory-reared An. stephensi were characterized for biological forms based on the number of ridges on the egg s float. DNA sequencing of the partial AsteObp1 gene of An. stephensi individuals were performed by Sangers method, either directly or after cloning with a plasmid vector. Additionally, AsteObp1 sequences of various laboratory lines of An. stephensi were retrieved from a public sequence database. ResultsAsteObp1 intron-1 in Indian An. stephensi populations are highly polymorphic with the presence of more than 13 haplotypes exhibiting nucleotides as well as length-polymorphism (90-to-121 bp). No specific haplotype or a group of closely related haplotypes of intron-1 was found associated with any biological form identified morphologically. High heterozygosity for this marker with a low inbreeding coefficient in field and laboratory populations indicates that this marker is not suitable for the delimitation of putative sibling species, at least in Indian populations. ConclusionsAsteObp1 cannot serve as a marker for identifying biological forms of An. stephensi or putative sibling species in Indian populations.

molecular biology↗

bioRxiv2021

Programmed cell death recruits macrophages into the developing mouse cochlea

Programmed cell death (PCD) plays a critical role in the development and maturation of the cochlea. Significant remodeling occurs among cells of the greater epithelial ridge (GER) of Kollikers organ, leading to tissue regression and formation of the inner sulcus. In mice, this event normally occurs between postnatal days 5-15 (P5-15) and is regulated by thyroid hormone (T3). During this developmental time period, the cochlea also contains a large population of macrophages. Macrophages are frequently involved in the phagocytic clearance of dead cells, both during development and after injury, but the role of macrophages in the developing cochlea is unknown. This study examined the link between developmental cell death in the GER and the recruitment of macrophages into this region. Cell death in the basal GER begins at P5 and enhanced numbers of macrophages were observed at P7. This pattern of macrophage recruitment was unchanged in mice that were genetically deficient for CX3CR1, the receptor for fractalkine (a known macrophage chemoattractant). We found that injection of T3 at P0 and P1 caused GER cell death to begin at P3, and this premature PCD was accompanied by earlier recruitment of macrophages. We further found that depletion of macrophages from the developing cochlea (using CX3CR1DTR/+ mice and treatment with the CSF1R antagonist BLZ945) had no effects on the pattern of GER regression. Together, these findings suggest that macrophages are recruited into the GER region after initiation of developmental PCD, but that they are not essential for GER regression during cochlear remodeling.

developmental biology↗

bioRxiv2021

Guidelines for reliable and reproducible functional enrichment analysis

Gene set enrichment tests (a.k.a. functional enrichment analysis) are among the most frequently used methods in computational biology. Despite this popularity, there are concerns that these methods are being applied incorrectly and the results of some peer-reviewed publications are unreliable. These problems include the use of inappropriate background gene lists, lack of false discovery rate correction and lack of methodological detail. An example analysis of public RNA-seq reveals that these methodological errors alter enrichment results dramatically. To ascertain the frequency of these errors in the literature, we performed a screen of 186 open access research articles describing functional enrichment results. We find that 95% of analyses using over-representation tests did not implement an appropriate background gene list or did not describe this in the methods. Failure to perform p-value correction for multiple tests was identified in 43% of analyses. Many studies lacked detail in the methods section about the tools and gene sets used. Only 15% of studies avoided major flaws, which highlights the poor state of functional enrichment rigour and reporting in the contemporary literature. We provide a set of minimum standards that should act as a checklist for researchers and peer-reviewers.

bioinformatics↗

bioRxiv2021

FUS Oncofusion Protein Condensates Recruit mSWI/SNF Chromatin Remodelers via Heterotypic Interactions Between Prion-like Domains

Fusion transcription factors generated by genomic translocations are common drivers of several types of cancers including sarcomas and leukemias. Oncofusions of the FET (FUS, EWSR1, and TAF15) family of proteins result from fusion of the prion-like domain (PLD) of FET proteins to the DNA-binding domain (DBD) of certain transcription regulators and are implicated in aberrant transcriptional programs through interactions with chromatin remodelers. Here, we show that FUS-DDIT3, a FET oncofusion protein, undergoes PLD-mediated phase separation into liquid-like condensates. Nuclear FUS-DDIT3 condensates can recruit essential components of the global transcriptional machinery such as the chromatin remodeler SWI/SNF. The recruitment of mammalian SWI/SNF is driven by heterotypic PLD-PLD interactions between FUS-DDIT3 and core subunits of SWI/SNF, such as the catalytic component BRG1. Further experiments with single-molecule correlative force-fluorescence microscopy support a model wherein the fusion protein forms condensates on DNA surface and enrich BRG1 to activate transcription by ectopic chromatin remodeling. Similar PLD-driven co-condensation of mSWI/SNF with transcription factors can be employed by other oncogenic fusion proteins with a generic PLD-DBD domain architecture for global transcriptional reprogramming.

biophysics↗

bioRxiv2020

Sequence-encoded and Composition-dependent Protein-RNA Interactions Control Multiphasic Condensate Topologies

Multivalent protein-protein and protein-RNA interactions are the drivers of biological phase separation. Biomolecular condensates typically contain a dense network of multiple proteins and RNAs, and their competing molecular interactions play key roles in regulating the condensate composition and structure. Employing a ternary system comprising of a prion-like polypeptide (PLP), arginine-rich polypeptide (RRP), and RNA, we show that competition between the PLP and RNA for a single shared partner, the RRP, leads to RNA-induced demixing of PLP-RRP condensates into stable coexisting phases-homotypic PLP condensates and heterotypic RRP-RNA condensates. The morphology of these biphasic condensates (non-engulfing/ partial engulfing/ complete engulfing) is determined by the RNA-to-RRP stoichiometry and the hierarchy of intermolecular interactions, providing a glimpse of the broad range of multiphasic patterns that are accessible to these condensates. Our findings provide a minimal set of physical rules that govern the composition and spatial organization of multicomponent and multiphasic biomolecular condensates.

biophysics↗

bioRxiv2020

Dynamic patterns of YAP1 expression and cellular localization in the developing and injured utricle

The Hippo pathway is an evolutionarily conserved signaling pathway involved in regulating organ size, development, homeostasis and regeneration1-4. YAP1 is a transcriptional coactivator and the primary effector of Hippo signaling. Upstream activation of the Hippo pathway leads to nuclear translocation of YAP1, which then evokes changes in gene expression and cell cycle entry5. A prior study has demonstrated nuclear translocation of YAP1 in the supporting cells of the developing utricle6, but the possible role of YAP1 in hair cell regeneration is unclear. The present study characterizes the cellular localization of YAP1 in the utricles of mice and chicks, both under normal conditions and after hair cell injury. During neonatal development of the mouse utricle, YAP1 expression was observed in the cytoplasm of supporting cells, and was also transiently expressed in the cytoplasm of hair cells. We also observed temporary nuclear translocation of YAP1 in supporting cells of the mouse utricle at short time periods after placement in organotypic culture. However, little or no nuclear translocation of YAP1 was observed after injury to the utricles of neonatal or mature mice. In contrast, a significant degree of YAP1 nuclear translocation was observed in the chicken utricle after streptomycin-induced hair cell damage in vitro and in vivo. Together, these data suggest that differences in YAP1 signaling may be partly responsible for the distinct regenerative abilities of the avian vs. mammalian inner ear.

cell biology↗

bioRxiv2020

Persistence and stability of interacting species in response to climate warming: The role of trophic structure

Over the past century, the Earth has experienced roughly 0.4-0.8{degrees}C rise in the average temperature and which is projected to increase between 1.4-5.8{degrees}C by the year 2100. The increase in the Earths temperature directly influences physiological traits of individual species in ecosystems. However, the effect of these changes in community dynamics, so far, remains relatively unknown. Here we show that the consequences of warming (i.e., increase in the global mean temperature) on the interacting species persistence or extinction are correlated with their trophic complexity and community structure. In particular, we investigate different nonlinear bioenergetic tri-trophic food web modules, commonly observed in nature, in the order of increasing trophic complexity; a food chain, a diamond food web and an omnivorous interaction. We find that at low temperatures, warming can destabilize the species dynamics in the food chain as well as the diamond food web, but it has no such effect on the trophic structure that involves omnivory. In the diamond food web, our results indicate that warming does not support top-down control induced co-existence of intermediate species. However, in all the trophic structures warming can destabilize species up to a threshold temperature. Beyond the threshold temperature, warming stabilizes species dynamics at the cost of the extinction of higher trophic species. We demonstrate the robustness of our results when a few system parameters are varied together with the temperature. Overall, our study suggests that variations in the trophic complexity of simple food web modules can influence the effects of climate warming on species dynamics.

ecology↗