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Patil, S.

Publications and source records attributed to Patil, S..

44 records · Page 3Linked to original sources

Arabidopsis ACINUS is O-glycosylated and regulates transcription and alternative splicing of regulators of reproductive transitions

O-GlcNAc modification plays important roles in metabolic regulation of cellular status. Two homologs of O-GlcNAc transferase, SECRET AGENT (SEC) and SPINDLY (SPY), which have O-GlcNAc and O-fucosyl transferase activities, respectively, are essential in Arabidopsis but have largely unknown cellular targets. Here we show that AtACINUS is O-GlcNAcylated and O-fucosylated and mediates regulation of transcription, alternative splicing (AS), and developmental transitions. Knocking-out both AtACINUS and its distant paralog AtPININ causes severe growth defects including dwarfism, delayed seed germination and flowering, and abscisic acid (ABA) hypersensitivity. Transcriptomic and protein-DNA/RNA interaction analyses demonstrate that AtACINUS represses transcription of the flowering repressor FLC and mediates AS of ABH1 and HAB1, two negative regulators of ABA signaling. Proteomic analyses show AtACINUSs O-GlcNAcylation, O-fucosylation, and association with splicing factors, chromatin remodelers, and transcriptional regulators. Some AtACINUS/AtPININ-dependent AS events are altered in the sec and spy mutants, demonstrating a function of O-glycosylation in regulating alternative RNA splicing.

molecular biology↗

Structure of the ALS Mutation Target Annexin A11 Reveals a Stabilising N-Terminal Segment

The functions of the annexin family of proteins involve binding to Ca2+, lipid membranes, other proteins, and RNA, and the annexins share a common folded core structure at the C terminus. Annexin A11 (AnxA11) has a long N-terminal region, which is predicted to be disordered, binds RNA, and forms membraneless organelles involved in neuronal transport. Mutations in AnxA11 have been linked to amyotrophic lateral sclerosis (ALS). We studied the structure and stability of AnxA11 and identified a short stabilising segment in the N-terminal end of the folded core, which links domains I and IV. Crystal structure of the AnxA11 core highlights main-chain hydrogen bonding interactions formed through this bridging segment, which are likely conserved in most annexins. The structure was also used to study the currently known ALS mutations in AnxA11. Three of these mutations correspond to buried Arg residues highly conserved in the annexin family, indicating central roles in annexin folding. The structural data provide starting points for detailed structure-function studies of both full-length AnxA11 and the disease variants being identified in ALS.

biochemistry↗

Differential tissue stiffness of body column facilitates locomotion of Hydra on solid substrates

The bell-shaped members of Cnidaria typically move around by swimming, whereas the Hydra polyp can perform locomotion on solid substrates in aquatic environment. To address the biomechanics of locomotion on rigid substrates, we studied the somersaulting locomotion in Hydra. We applied atomic force microscopy to measure the local mechanical properties of Hydras body column and identified the existence of differential Youngs modulus between the shoulder region versus rest of the body column at 3:1 ratio. We show that somersault primarily depends on differential tissue stiffness of the body column and is explained by computational models that accurately recapitulate the mechanics involved in this process. We demonstrate that perturbation of the observed stiffness variation in the body column by modulating the extracellular matrix (ECM) polymerization impairs the somersault movement. These results provide mechanistic basis for the evolutionary significance of differential extracellular matrix properties and tissue stiffness.

biophysics↗

Assessing the in vitro resistance development in Enterovirus 71 in the context of combination antiviral treatment

There are currently no antivirals available to treat infection with enterovirus A71 (EV-A71) or any other enterovirus. The extensively studied capsid binders select rapidly for drug-resistant variants. We here explore whether the combination of two direct-acting enterovirus inhibitors with a different mechanism of action may delay or prevent resistance development to the capsid binders. To that end, the in vitro dynamics of resistance development to the capsid binder pirodavir was studied either alone or in combination with (i) a viral 2C-targeting compound (SMSK_0213), (ii) a viral 3C-protease inhibitor (rupintrivir) or (iii) a viral RNA-dependent RNA polymerase (RdRp) inhibitor [7-deaza-2C-methyladenosine (7DMA)]. We demonstrate that combining pirodavir with either rupintrivir or the nucleoside analogue 7DMA delays the development of resistance to pirodavir and that no resistance to the protease or polymerase inhibitor develops. The combination of pirodavir with the 2C inhibitor results in a double-resistant virus population. The deep sequencing analysis of resistant populations revealed that even though resistant mutations are present in less than 30% of the population, this still provides the resistant phenotype.

microbiology↗

Cancer PRSweb - an Online Repository with Polygenic Risk Scores (PRS) for Major Cancer Traits and Their Phenome-wide Exploration in Two Independent Biobanks

To facilitate scientific collaboration on polygenic risk scores (PRS) research, we created an extensive PRS online repository for 49 common cancer traits integrating freely available genome-wide association studies (GWAS) summary statistics from three sources: published GWAS, the NHGRI-EBI GWAS Catalog, and UK Biobank-based GWAS. Our framework condenses these summary statistics into PRS using various approaches such as linkage disequilibrium pruning / p-value thresholding (fixed or data-adaptively optimized thresholds) and penalized, genome-wide effect size weighting. We evaluated the PRS in two biobanks: the Michigan Genomics Initiative (MGI), a longitudinal biorepository effort at Michigan Medicine, and the population-based UK Biobank (UKB). For each PRS construct, we provide measures on predictive performance, calibration, and discrimination. Besides PRS evaluation, the Cancer-PRSweb platform features construct downloads and phenome-wide PRS association study results (PRS-PheWAS) for predictive PRS. We expect this integrated platform to accelerate PRS-related cancer research.

genetics↗

Antidepressants act by binding to the cholesterol-interaction site at TRKB neurotrophin receptor

It is unclear how binding of antidepressant drugs to their targets gives rise to the clinical antidepressant effect. We discovered that the transmembrane domain of TRKB, the brain-derived neurotrophic factor (BDNF) receptor that promotes neuronal plasticity and antidepressant responses, has a cholesterol-sensing function that mediates synaptic effects of cholesterol. We then found that both typical and fast-acting antidepressants directly bind to TRKB, thereby facilitating synaptic localization of TRKB and its activation by BDNF. Extensive computational approaches including atomistic molecular dynamics simulations revealed a binding site at the transmembrane region of TRKB dimers. Mutation of the TRKB antidepressant-binding motif impaired cellular, behavioral and plasticity-promoting responses to antidepressants in vitro and in vivo. We suggest that binding to TRKB and the allosteric facilitation of BDNF signaling is the common mechanism for antidepressant action, which proposes a framework for how molecular effects of antidepressants are translated into clinical mood recovery.

neuroscience↗

Poly-Enrich: Count-based Methods for Gene Set Enrichment Testing with Genomic Regions and Updates to ChIP-Enrich

Gene set enrichment (GSE) testing enhances the biological interpretation of ChIP-seq data and other large sets of genomic regions. Our group has previously introduced two GSE methods for genomic regions: ChIP-Enrich for narrow regions and Broad-Enrich for broad genomic regions, such as histone modifications. Here, we introduce new methods and extensions that more appropriately analyze sets of genomic regions with vastly different properties. First, we introduce Poly-Enrich, which models the number of peaks assigned to a gene using a generalized additive model with a negative binomial family to determine gene set enrichment, while adjusting for gene locus length (#bps associated with each gene). This is the first method that controls for locus length while accounting for the number of peaks per gene and variability among genes. We also introduce a flexible weighting approach to incorporate region scores, a hybrid enrichment approach, and support for new gene set databases and reference genomes/species. As opposed to ChIP-Enrich, Poly-Enrich works well even when nearly all genes have a peak. To illustrate this, we used Poly-Enrich to characterize the pathways and types of genic regions (introns, promoters, etc) enriched with different families of repetitive elements. By comparing ChIP-Enrich and Poly-Enrich results from ENCODE ChIP-seq data, we found that the optimal test depends more on the pathway being regulated than on the transcription factor or other properties of the dataset. Using known transcription factor functions, we discovered clusters of related biological processes consistently better modeled with either the binary score method (ChIP-Enrich) or count based method (Poly-Enrich). This suggests that the regulation of certain processes is more often modified by multiple binding events (count-based), while others tend to require only one (binary). Our new hybrid method handles this by automatically choosing the optimal method, with correct FDR-adjustment. Author SummaryAlthough every cell in our body contains the same DNA, our cells perform vastly different functions due to differences in how our genes are regulated. Certain regions of the genome are bound by DNA binding proteins (transcription factors), which regulate the expression of nearby genes. After an experiment to identify a large set of these regions, we can then model the association of these regions with various cellular pathways and biological processes. This analysis helps understand the overall biological effect that the binding events have on the cells. For example, if genes relating to apoptosis tend to have the transcription factor, Bcl-2, bind more often nearby, then Bcl-2 is likely to have a vital role in regulating apoptosis. The specifics of how to best perform this analysis is still being researched and depends on properties of the set of genomic regions. Here, we introduce a new, more flexible method that counts the number of occurrences per gene and models that in a sophisticated statistical test, and compare it to a previous method. We show that the optimal method depends on multiple factors, and the new method, Poly-Enrich, allows interesting findings in scenarios where the previous method failed.

bioinformatics↗

High rates of human faecal carriage of mcr-1-positive multi-drug resistant isolates emerge in China in association with successful plasmid families

SynopsisO_ST_ABSBackgroundC_ST_ABSmcr-1-mediated transmissible colistin resistance in Enterobacteriaceae is concerning, given colistin is frequently used as a treatment of last resort in multidrug-resistant Enterobacteriaceae infections. Reported rates of human mcr-1 gastrointestinal carriage have historically been low.\n\nObjectivesTo identify trends in human gastrointestinal carriage of mcr-1 positive and mcr-1-positive/cefotaxime-resistant Enterobacteriaceae in Guangzhou, China, 2011-2016, and investigate the genetic contexts of mcr-1 in a subset of mcr-1-positive/cefotaxime-resistant strains using whole genome sequencing (WGS).\n\nMethodsOf 8,022 faecal samples collected, 497 (6.2%) were mcr-1- positive, and 182 (2.3%) mcr-1-positive/cefotaxime-resistant. Trends in carriage were assessed using iterative sequential regression. A subset of mcr-1-positive isolates was sequenced (Illumina), and genetic contexts of mcr-1 were characterised.\n\nResultsWe observed marked increases in mcr-1 (now ~30% prevalence) and more recent (since January 2014) increases in mcr-1-positive/third-generation cephalosporin-resistant Enterobacteriaceae human colonisation (p<0.001). Sub-cultured mcr-1-positive/third-generation cephalosporin-resistant isolates were commonly multi-drug resistant.\n\nWGS of 50 mcr-1/third-generation cephalosporin-resistant isolates (49 Escherichia coli; 1 Klebsiella pneumoniae) demonstrated bacterial strain diversity (39 E. coli sequence types); mcr-1 in association with common plasmid backbones (IncI, IncHI2/HI2A, IncX4) and sometimes in multiple plasmids; frequent mcr-1 chromosomal integration; and loss of the mcr-1-associated insertion sequence ISApl1 in some plasmids. Significant sequence similarity with published mcr-1 plasmid sequences was consistent with spread amongst pig, chicken and human reservoirs.\n\nConclusionsThe high positivity rate (~10%) of mcr-1 in multidrug-resistant E. coli colonising humans is a clinical threat; the diverse genetic mechanisms (strains/plasmids/insertion sequences) associated with mcr-1 have likely contributed to its dissemination, and will facilitate its persistence.

microbiology↗