Biology subjects

Islam, Z.

Publications and source records attributed to Islam, Z..

10 recordsLinked to original sources

bioRxiv2026

Phenotypic and Molecular Characterization of Potentially New Shigella boydii Serotype in Bangladesh

Objective: Shigella is a major cause of bacillary dysentery among children under 5 years of age, especially in low- and middle-income countries. At Dhaka hospital of icddr,b, every year around 3% of Shigella isolates from patients with diarrhea are identified as Shigella-like organisms (SLOs). These isolates do not react with any of the existing and provisional Shigella antisera. The major aims of the present study were to characterize a unique cluster of SLOs using phenotypic and genotypic methods. Methods: A cluster of 6 SLOs was characterized using biochemical tests, serotyping, antimicrobial susceptibility, and virulence assay by using the Sereny test, PCR and compared their pulsed-field gel electrophoresis (PFGE) patterns with known serotypes of Shigella spp. Antisera against the isolate were raised in a rabbit model to determine cross-reactivity with known serotypes. Results: All six SLOs were mannitol fermenting, have invasive properties, positive for ipaH and Shigella enterotoxin 2 gene along with possession of virulence plasmid of ~ 140 MDa. All isolates were resistant to ampicillin, tetracycline, sulfamethoxazole-trimethoprim, but were sensitive to mecillinam, nalidixic acid, and ciprofloxacin. Plasmid and PFGE profiles showed that the genomic patterns of these isolates were identical but were different from all other S. boydii serotypes. Antiserum prepared against one of the isolates agglutinated with all isolates but did not cross-react with other Shigella and E. coli reference strains. Conclusion: This unique cluster of isolates might belong to a new provisional serovar of S. boydii and further analysis is required to incorporate it into the stereotypic scheme of Shigella.

microbiology↗

bioRxiv2026

Pseudoarthrobacter BD237 volatile organic compounds promote Brachypodium distachyon growth

Microbial volatile organic compounds (mVOCs) present an environmentally sustainable alternative or supplement to traditionally used agrochemicals, such as fertilisers, herbicides and pesticides. Microbial VOCs can promote the growth and stress tolerance of a variety of dicot plants, largely through modulation of phytohormone pathways. However, their effect in monocot plants, particularly grasses, remains largely unexplored. PseudoarthrobacterBD237s mVOCs were assayed for their growth promoting effect in the model cereal, Brachypodium distachyon. BD237 mVOCs were found to significantly increase the dry shoot and root weight of B. distachyon by 25% and 42%, respectively. Gas chromatography analysis showed that BD237 produced a variety of alcohols and ketones. Exposure to pure standards of phenylethyl alcohol and 2-nonanone were found to significantly promote B. distachyon growth. Transcriptome analysis of B.distachyon roots exposed to BD237 mVOC revealed significant upregulation of genes related to photosynthesis and response to abiotic stress. Transcriptome analysis of BD237 plate colonies exposed to B. distachyon VOCs revealed no significant differential transcription, indicating that BD237 VOC production may be constitutive. These results suggest that BD237 mVOCs may promote B. distachyon growth by increasing photosynthetic rate and may increase tolerance to abiotic stressors such as salinity and drought. Collectively, this work expands our understanding of microbe monocot VOC mediated interactions and identifies specific VOCs as potential grass biostimulants.

microbiology↗

bioRxiv2026

Comparative Genomic and Epigenetic Landscape of Histone H3.3 G34R and K27M-Mutated Pediatric High-Grade Glioma Suggests Divergent Precision Oncology Strategies

Histone H3-G34R and H3-K27M mutations define distinct diffuse high-grade glioma subtypes diffuse hemispheric glioma (DHG), midline (DMG), and pontine gliomas (DIPG). We characterized pathway-architectures using cBioPortal and pedcBioPortal for H3-G34R (n=112) and H3-K27M (n=727) mutated-gliomas, co-mutations, copy numbers (CNA), and variant data (n=112/727, n=86/578, n=51/313). We evaluated altered-genes as oncogenic by OncoKB, Gene-Ontology (GO) heatmaps and process-enrichment using clusterProfiler (Benjamini-Hochberg-adjusted p<0.05). H3-G34R-gliomas harbored near-universal TP53 (94.1%), ATRX (81.4%) co-mutations and PDGFRA alteration (54.9% mutation; 17.1% amplification) within 4q12 amplicon that includes KIT and KDR. Pathway-enrichment converged on G1/S cell-cycle checkpoints, and epigenetic regulation, driven principally by TP53, ATRX, PTEN, BCOR, TERT, FBXW7, and PPM1D. CDK6 amplification was rare (2.6%), despite H3-G34R association with CDK6-dependency including benefit from CDK4/6 inhibition. H3-K27M-gliomas displayed PI3K/AKT pathway activation (PIK3CA, 14.9%; NF1, 13.3%; PDGFRA, 10.8%, PIK3R1, 7.8%; PTEN, 5.7%) and developmental signatures through NF1, PTEN, and SOX10 (4.95%) mutations. TP53 (62.2%) and ATRX (21.2%) co-mutations were less frequent in H3-K27M versus H3-G34R, while PPM1D was H3-K27M-enriched (19.3%). MGMT promoter methylation occurred frequently in H3-G34R (65.2%, 15/23) versus H3-K27M-gliomas (5.4%, 4/74), despite genome-hypomethylation of H3-G34R. H3-G34R-gliomas, unlike H3-K27M, upregulated ganglionic GSX2, DLX1, DLX2, and FOXG1. SOX10 was upregulated in H3-K27M-gliomas, versus H3-G34R. Lack of MGMT methylation in H3-K27M-gliomas correlates with temozolomide resistance; we previously reported imipridones ONC201/ONC206 reduce MGMT, EZH1 and EZH2 expression in H3-K27M-glioma cells. Divergent PDGFRA-mutations among MGMT-methylated versus unmethylated H3-G34R-gliomas warrants investigation of PDGFRA-signaling and epigenetic regulation. Our findings suggest divergent precision oncology therapeutic strategies to exploit unique vulnerabilities in H3-K27M and H3-G34R-gliomas.

cancer biology↗

bioRxiv2026

Autoantibodies from recovered Guillain-Barre syndrome patients exhibit altered effector functions that prevent subsequent neuron degeneration

Guillain-Barre syndrome (GBS) is an autoimmune polyneuropathy that is the leading cause of nonpoliovirus-associated acute flaccid paralysis worldwide. In most cases, GBS occurs following an infection, most commonly Campylobacter jejuni, through the induction of antibodies recognizing bacterial ganglioside-mimicking lipooligosaccharides that cross-react with human neuronal gangliosides. This post-infectious autoimmune cascade causes neuropathy, from which patients can recover as their anti-ganglioside antibody titers diminish and immunostimulation decreases. In this study, we find 10% of clinically confirmed GBS patients maintain high titers of circulating anti-ganglioside antibodies more than one decade after recovery. These antibodies no longer cause neuropathy compared to acute sera from the same patients using a human pluripotent stem cell-derived sensory neuron model with human complement. We found both IgG subclass and glycoform differences between paired acute and recovered GBS patient sera, including anti-inflammatory modifications on isolated anti-GM1 ganglioside antibodies. Together, these data suggest that patients with GBS select for non-pathogenic variants of autoantibodies that are no longer capable of damaging their neurons, but may still protect against C. jejuni infection.

immunology↗

bioRxiv2025

One-Pot Isothermal Linear Amplification and Cas12a-based Nucleic Acid Detection

CRISPR-based nucleic acid diagnostics are a promising class of point-of-care tools that could dramatically improve healthcare outcomes for millions worldwide. However, these diagnostics require nucleic acid pre-amplification, an additional step that complicates deployment to low resource settings. Here, we developed CATNAP (Cas trans-nuclease detection of amplified products), a method that integrates isothermal linear DNA amplification with Cas12a detection in a single reaction. CATNAP uses a nicking enzyme and DNA polymerase to continuously generate single-stranded DNA, activating Cas12as trans-cleavage activity without damaging the template. We optimized enzyme combinations, buffer conditions, and target selection to achieve high catalytic efficiency. CATNAP successfully distinguished between high- and low-risk HPV strains and detects HPV-16 in a cervical cancer crude cell lysate at room temperature with minimal equipment, offering advantages over PCR-based approaches. We conclude that CATNAP bridges the sensitivity gap in CRISPR diagnostics while maintaining simplicity, making accurate disease detection more accessible in resource-limited settings.

biochemistry↗

bioRxiv2024

Acute Activation of Genes Through Transcriptional Condensates Impact Non-target Genes in a Chromatin Domain

Transcription activation of genes by estrogen is driven by enhancers, which are often located within the same Topologically Associating Domain (TAD) as non-targeted promoters. We investigated how acute enhancer-driven activation affects neighbouring non-target genes within the same TAD. Using single-molecule RNA FISH (smFISH), we tracked the transcription of TFF1 (enhancer-target gene) and TFF3 (non-target gene) during estrogen stimulation. We observed mutually exclusive expression patterns: TFF1 expression peaked at 1 hour, while TFF3 reached its peak at 3 hours, after TFF1 activation had diminished. Chromatin looping data indicated that the enhancer loops with TFF1 but not TFF3, suggesting that TFF3 upregulation is not due to direct enhancer-promoter interactions. CRISPR deletion of the enhancer, affected TFF1 transcription more acutely than TFF3. 1,6-hexanediol (HD) exposure suggested that the TFF1 enhancer:promoter undergo a potential ER-mediated condensate formation, which sequesters the transcriptional machinery and inhibits TFF3 expression. As estrogen signalling fades at 3h, TFF1 expression declines while TFF3 expression increases. Our findings reveal that enhancer-driven activation can indirectly repress neighbouring genes within the same TAD, highlighting a dynamic shift in gene expression as signalling progresses.

molecular biology↗

bioRxiv2024

Clubroot disease in soil: An examination of its occurrence in chemical and organic environments

Clubroot is a disease in cruciferous plants caused by the soil-borne pathogen Plasmodiophora brassicae. This pathogen rapidly spreads in soil, and plant growth is inhibited by infection with spores. In this study, the development of clubroot disease in Brassica rapa var. perviridis was investigated in different soil environments (chemical and organic soils). The bacterial biomass and diversity of the soil and roots were also analyzed in both chemical and organic soils. Bacterial biomass and diversity in the organic soil were higher than those in the chemical soil. The disease severity of plants cultivated in organic soil was lower than that in chemical soil. The number of endophytic bacteria in the roots decreased when the plants were infected with P. brassicae in both soil types. Higher bacterial biomass in the soils and roots appeared to reduce the infection of P. brassicae. ImportancClubroot is a major disease of cruciferous plants caused by soil borne pathogen Plasmodiophora brassica. Pesticides are applied in the soil during cultivation for the inhibition of clubroot disease, which demise soil microbiome. Therefore, eco-friendly control methods are required for sustainable cultivation. Soil management is an important strategy to inhibit clubroot disease severity. In this study, the occurrence of clubroot disease in B.rapa were compared in two distinct soil environments (chemical and organic). Results show infection rate increased with the increase of spore number for both chemical and organic soil environments. However, the diseases severity was lower in plants cultivated in organic soil. The higher endophytic bacterial biomass and diversity seems to be linked for the disease inhibition in organic plants. These findings suggest a sustainable soil management process to reduce clubroot disease prevalence. Application of organic fertilizers in commented soils could substantially reduce clubroot disease severity in the plants.

microbiology↗

bioRxiv2024

MATRIN3 deficiency triggers autoinflammation via cGAS-STING activation

Interferon-stimulated genes (ISGs) comprise a program of immune effectors important for host immune defense. When uncontrolled, ISGs play a central role in interferonopathies and other inflammatory diseases. The mechanisms responsible for turning on ISGs are not completely known. By investigating MATRIN3 (MATR3), a nuclear RNA-binding protein mutated in familial ALS, we found that perturbing MATR3 results in elevated expression of ISGs. Using an integrative approach, we elucidate a pathway that leads to activation of cGAS-STING. This outlines a plausible mechanism for pathogenesis in a subset of ALS, and suggests new diagnostic and therapeutic approaches for this fatal disease. One-Sentence SummaryMis-splicing of Tudor Domain Containing 3 (TDRD3) in the absence of MATR3 unleashes R-loops and interferon-stimulated genes.

molecular biology↗

bioRxiv2021

Active enhancers strengthen TAD insulation by bRNA mediated CTCF enrichment at the TAD boundaries

Vertebrate genomes are partitioned into Topologically Associating Domains (TADs), which are typically bound by head-to-head pairs of CTCF binding sites. Transcription at TAD boundaries correlates with better insulation, however, it is not known whether the boundary transcripts themselves contribute to boundary function. Here we characterize boundary-associated RNAs genome-wide, focusing on the disease-relevant INK4a/ARF TAD. Using CTCF site deletions and boundary-associated RNA knockdowns, we observe that boundary-associated RNAs facilitate recruitment and clustering of CTCF at TAD borders. The resulting CTCF enrichment enhances TAD insulation, enhancer:promoter interactions and TAD gene expression. Importantly, knockdown of boundary-associated RNAs results in loss of boundary insulation function. Using enhancer deletions and CRISPRi of promoters we show that active TAD enhancers but not promoters induce boundary-associated RNA transcription, thus defining a novel class of regulatory enhancer RNAs.

genomics↗

bioRxiv2019

Ligand dependent gene regulation by transient ER clustered enhancers

Unliganded nuclear receptors have been implicated in ligand-dependent gene regulation. However, the underlying mechanisms are not fully understood. Here we demonstrate that unliganded ER binds to specific sites in the genome thereby pre-marking them as future functional enhancers. Upon ligand exposure, ER binds to several EREs relatively proximal to the pre-marked, or persistent, ER-bound sites. Interestingly, the persistent sites interact extensively, via chromatin looping, with the proximal transiently bound sites forming ER clustered enhancers in 3D. CRISPR-based deletion of TFF1 persistent site disrupts the formation of its clustered enhancer resulting in the loss of E2-dependent induced expression of TFF1 and its neighboring genes within the same cluster. The clustered enhancers overlap with nuclear ER puncta that coalesce in a ligand-dependent manner. Furthermore, formation of clustered enhancers, as well as puncta, coincide with the active phase of signaling and their later disappearance results in the loss of gene expression even though persistent sites remain bound by ER. Our results establish the role of persistent unliganded ER binding in priming enhancer clusters in 3D that drive transient, but robust, gene expression in a ligand-dependent fashion.

molecular biology↗