Biology subjects

Saini, P.

Publications and source records attributed to Saini, P..

4 recordsLinked to original sources

bioRxiv2023

Restriction of the growth and biofilm formation of ESKAPE pathogens by caprine gut-derived probiotic bacteria

The accelerated rise of antimicrobial resistance (AMR) poses a significant global health risk, necessitating the exploration of alternative strategies for combating pathogenic infections. Biofilm-related infections, which are unresponsive to standard antibiotics, often require the use of higher-order antimicrobials with toxic side effects and a potential for disrupting the microbiome. Probiotic therapy, with its diverse benefits and inherent safety, is emerging as a promising approach for preventing and treating various infections and as an alternative to antibiotic therapy. In this study, we isolated novel probiotic bacteria from the gut of domestic goats (Capra hircus) and evaluated their antimicrobial and antibiofilm activities against the ESKAPE group of pathogens. We performed comprehensive microbiological, biochemical, and molecular characterizations, including analysis of the 16S-rRNA gene V1-V3 region and the 16S-23S ISR region, on 20 caprine gut-derived lactic acid bacteria (LAB). Among these, six selected LABs demonstrated substantial biofilm formation in anaerobic conditions, and exhibited robust cell surface hydrophobicity and autoaggregation properties highlighting their superior enteric colonization capability. Notably, these LAB isolates exhibited broad-spectrum growth inhibitory and anti-biofilm properties against ESKAPE pathogens. Additionally, the LAB isolates were susceptible to antibiotics listed by the European Food Safety Authority (EFSA), within the prescribed Minimum Inhibitory Concentration limits, suggesting their safety as feed additives. The remarkable probiotic characteristics exhibited by the caprine gut-derived LAB isolates in this study strongly endorse their potential as compelling alternatives to antibiotics and as direct-fed microbial (DFM) feed supplements in the livestock industry, addressing the escalating need for antibiotic-free animal products.

microbiology↗

bioRxiv2023

SUMO protease FUG1, histone reader AL3 and the PRC1 Complex are integral to repeat-expansion induced epigenetic silencing in Arabidopsis thaliana

Epigenetic gene silencing induced by expanded repeats can cause diverse phenotypes ranging from severe growth defects in plants to genetic diseases such as Friedreichs ataxia in humans1. The molecular mechanisms underlying repeat expansion-induced epigenetic silencing remain largely unknown2,3. Using a plant model, we have previously shown that expanded repeats can induce smallRNAs which in turn can lead to epigenetic silencing through the RNA-dependent DNA methylation pathway4,5. Here, using a genetic suppressor screen, we confirm a key role for the RdDM pathway and identify novel components required for epigenetic silencing caused by expanded repeats. We show that FOURTH ULP LIKE GENE CLASS 1 (FUG1) - a SUMO protease, ALFIN-LIKE 3 - a histone reader and LIKE HETEROCHROMATIN 1 (LHP1) - a component of the PRC1 complex are required for repeat expansion-induced epigenetic silencing. Loss of any of these components suppress repeat expansion-associated phenotypes. SUMO protease FUG1 physically interacts with AL3 and perturbing its potential SUMOylation site disrupts its nuclear localisation. AL3 physically interacts with LHP1 of the PRC1 complex and the FUG1-AL3-LHP1 module is essential to confer repeat expansion-associated epigenetic silencing. Our findings highlight the importance post-translational modifiers and histone readers in epigenetic silencing caused by repeat expansions.

genetics↗

bioRxiv2022

The IPDGC/GP2 Hackathon - an open science event for training in data science, genomics, and collaboration using Parkinson's disease data

BackgroundOpen science and collaboration are necessary to facilitate the advancement of Parkinsons disease (PD) research. Hackathons are collaborative events that bring together people with different skill sets and backgrounds to generate resources and creative solutions to problems. These events can be used as training and networking opportunities. ObjectiveTo coordinate a virtual hackathon to develop novel PD research tools. Methods49 early career scientists from 12 countries collaborated in a virtual 3-day hackathon event in May 2021, during which they built tools and pipelines with a focus on PD. Resources were created with the goal of helping scientists accelerate their own research by having access to the necessary code and tools. ResultsEach team was allocated one of nine different projects, each with a different goal. These included developing post-genome-wide association studies (GWAS) analysis pipelines, downstream analysis of genetic variation pipelines, and various visualization tools. ConclusionHackathons are a valuable approach to inspire creative thinking, supplement training in data science, and foster collaborative scientific relationships, which are foundational practices for early career researchers. The resources generated can be used to accelerate research on the genetics of PD.

genetics↗

bioRxiv2022

SOX15 regulates stem cell pluripotency and promotes neural fate during differentiation by activating Hes5

SOX2 and SOX15 are Sox family transcription factors enriched in embryonic stem cells (ESCs). The role of SOX2 in activating gene expression programs essential for stem cell self-renewal and acquisition of pluripotency during somatic cell reprogramming is well-documented. However, the contribution of SOX15 to these processes is unclear and often presumed redundant with SOX2 largely because overexpression of SOX15 can partially restore self-renewal in SOX2-deficient ESCs. Here, we show that SOX15 contributes to stem cell maintenance by cooperating with ESC-enriched transcriptional coactivators to ensure optimal expression of pluripotency-associated genes. We demonstrate that SOX15 depletion compromises reprogramming of fibroblasts to pluripotency which cannot be compensated by SOX2. Ectopic expression of SOX15 promotes the reversion of a post-implantation, epiblast stem cell state back to a pre-implantation, ESC-like identity even though SOX2 is expressed in both cell states. We also uncover a role of SOX15 in lineage specification, by showing that loss of SOX15 leads to defects in commitment of ESCs to neural fates. SOX15 promotes neural differentiation by binding to and activating a previously uncharacterized distal enhancer of a key neurogenic regulator, Hes5. Together, these findings identify a multifaceted role of SOX15 in induction and maintenance of pluripotency and neural differentiation.

cell biology↗