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Ahmed, J.

Publications and source records attributed to Ahmed, J..

18 recordsLinked to original sources

Comparative immunogenicity and protective efficacy of formaldehyde-inactivated whole-cell and sonicated whole-cell extract vaccines against multidrug-resistant Pseudomonas aeruginosa in mice

Background: Pseudomonas aeruginosa is a major opportunistic Gram-negative pathogen responsible for healthcare-associated infections, while increasing antimicrobial resistance has narrowed therapeutic options. Vaccine development therefore represents an important complementary strategy for prevention. This study compared the immunogenicity and protective efficacy of a formaldehyde-inactivated whole-cell vaccine with a sonicated whole cell extract preparation against multidrug-resistant (MDR) P. aeruginosa in mouse model. Methods: Clinical P. aeruginosa isolates were obtained from specimens collected at Dhaka Medical College Hospital between July 2022 and February 2026. Formaldehyde-inactivated whole-cell and sonicated whole cell extract preparations were produced from P. aeruginosa. A total of 144 female Swiss albino mice aged 6-8 weeks were used: 120 mice were allocated to two independent immunization experiments and 24 mice were used for LD50 determination. Mice received three intramuscular immunizations on days 0, 14, and 28. Antigen-specific serum IgG was assessed by enzyme-linked immunosorbent assay (ELISA), functional antibody activity was evaluated by serum bactericidal assay (SBA), and protective efficacy was assessed following lethal intraperitoneal challenge. Results: Ten isolates from MDR P. aeruginosa were selected by simple random sampling from the clinical isolates for vaccine preparation. The estimated protein concentration of the sonicated preparation was 1.872 mg/mL. Both vaccine groups developed significantly higher anti-P. aeruginosa IgG responses than the control group after immunization (p<0.001). Following lethal challenge, survival was 100% in mice receiving the formaldehyde-inactivated vaccine and 91.7% among mice receiving the sonicated preparation; no control mice survived. Between-vaccine differences in survival were not statistically significant. SBA demonstrated complement-dependent bactericidal activity in sera from both vaccinated groups, with activity detectable to a dilution of 1:32 for the whole-cell vaccine and 1:64 for the sonicated preparation. Conclusions: Both vaccine preparations elicited strong humoral responses and substantial protection against lethal MDR P. aeruginosa challenge in mice. The findings support further investigation of multicomponent P. aeruginosa vaccine strategies, although additional studies using multiple challenge strains and broader immunological endpoints are required before conclusions regarding translational efficacy can be drawn.

microbiology↗

The role of reactive oxygen species and calcium signaling in antiviral defense in Arabidopsis

Plant viruses interfere with host signaling pathways, but it remains unclear how calcium (Ca2+) signaling, reactive oxygen species (ROS), and changes in the plasma membrane interact during viral infection. Here, we investigated how plantago asiatica mosaic virus (PlAMV) modulates host Ca2+ and ROS-associated signaling in Arabidopsis thaliana. Using live-cell imaging and the R-GECO1.2 Ca2+ sensor, we observed a rapid increase in cytoplasmic Ca2+ before the virus was detected, indicating that Ca2+ release occurs early in infection. Genetic analysis showed that GLR, CPK3, and CNGC, core components of Ca2+ signaling, limit PlAMV spread between cells, while the usual pattern-triggered immunity (PTI) co-receptors were not needed. This means that Ca2+-based antiviral restriction operates independently of PTI. With the plasma membrane-tethered and cytosolic HyPer7 biosensor, we found that ROS levels were lower inside infection foci in the inoculated leaves, but higher in nearby cells, respectively. The NADPH oxidases RBOHD and RBOHF, which produce ROS, slowed down the local viral propagation. The PM sphingolipid biosynthetic enzyme MOCA1 altered ROS patterns and reduced the viruss spread. Epistasis analysis revealed a functional interaction between RBOHD and MOCA1, suggesting that ROS signaling and plasma membrane sphingolipid homeostasis are interconnected in antiviral defense. Overall, our findings suggest that PlAMV triggers Ca2+ influx and ROS signaling at the plasma membrane, which induces sphingolipid reorganization and helps restrict the propagation of the virus. This study shows how Ca2+, ROS, and membrane sphingolipid signaling work together in plant antiviral immunity and points to possible ways to improve resistance to viruses.

plant biology↗

TNFR2 is Expressed by a Discrete Subset of Epidermal γ δ T Cells with an IL-17 Gene Signature during Psoriasis

Psoriasis is a chronic skin disease that results in scaly patches and affects 2-3% of people worldwide. Therapeutic treatment targets the TNF-/IL-17 axis to disrupt keratinocyte hyperproliferation and inflammation. While more is known about the role of dermal {beta} and {gamma}{delta} T cells in IL-17 production, less is understood about the role of resident epidermal T cells. Here, we examine how TNF- modulates epidermal {gamma}{delta} T cell activation and function. We show that a subset of activated epidermal {gamma}{delta} T cells expresses TNFR2 with or without TNFR1. Stimulation with TNF- induces epidermal {gamma}{delta} T cells to produce IL-17 family cytokines and chemokines. Epidermal {gamma}{delta} T cells do not require TNFR1 or 2 for development or homing to the skin. Instead, TNFR2 plays roles in epidermal {gamma}{delta} T cell function skewing them toward a T{gamma}{delta}17 phenotype during psoriasis. Investigation of the mechanisms by which TNF- associated inflammation impacts epidermal {gamma}{delta} T cell function may help identify new cellular targets for immunotherapy or mark them as early regulators of skin inflammation.

immunology↗

Dendritic cells type 1 control the formation, maintenance, and function of tertiary lymphoidstructures in cancer

Tertiary lymphoid structures (TLS) are organized immune cell aggregates that arise in chronic inflammatory conditions. In cancer, TLS are associated with better prognosis and enhanced response to immunotherapy, making these structures attractive therapeutic targets. However, the mechanisms regulating TLS formation and maintenance in cancer are incompletely understood. Using spatial transcriptomics and multiplex imaging across various human tumors, we found an enrichment of mature dendritic cells (DC) expressing high levels of CCR7 in TLS, prompting us to investigate the role of DC in the formation and maintenance of TLS in solid tumors. To address this, we developed a novel murine model of non-small cell lung cancer (NSCLC) that forms mature TLS, containing B cell follicles with germinal centers and T cell zones with T follicular helper cells (TFH) and TCF1+PD-1+ progenitor exhausted CD8+ T cells (Tpex). Here we show that, during the early stages of tumor development, TLS formation relies on IFN{gamma}-driven maturation of the conventional DC type 1 (cDC1) subset, their migration to tumor-draining lymph nodes (tdLN), and recruitment of activated T cells to the tumor site. As tumors progress, TLS maintenance becomes independent of T cell egress from tdLN, coinciding with a significant reduction of cDC1 migration to tdLN. Instead, mature cDC1 accumulate within intratumoral CCR7 ligand-enriched stromal hubs. Notably, timed depletion of cDC1 or disruption of their migration to these stromal hubs after TLS are formed alters TLS maintenance. Importantly, we found that cDC1-mediated antigen presentation to both CD4+ and CD8+ T cells and intact CD40 signaling, is critical for the maintenance of TLS, the preservation of the TFH cell pool, the formation of germinal center and the production of tumor-specific IgG antibodies. These findings underscore the key role of mature cDC1 in establishing and maintaining functional TLS within tumor lesions and highlight the potential for cDC1-targeting therapies as a promising strategy to enhance TLS function and improve anti-tumor immunity in patients with cancer.

immunology↗

Dendritic cells accelerate CAR T cells in irradiated tumors through chimeric synapses

The persistence of adoptively transferred T cells is vital for anti-tumor efficacy. Chimeric antigen receptor (CAR) T cells can persist indefinitely when delivered to patients with B cell cancers and can confer long-term remission. For patients with solid tumors, however, sustaining CAR T cell activity remains a major challenge. This has been attributed in part to the immune microenvironment within solid tumors, though the contribution of specific immune subsets to resistance to CAR T cells is not clear. Here we resolve how the immunology of irradiated tumors dramatically enhances persistence and efficacy of CAR T cells targeted to advanced lung metastases in a syngeneic mouse model. Remarkably, CAR T cell persistence depended critically on dendritic cells (DC) that underwent trogocytic "antigen-dressing" of tumor target antigens and stimulated CAR T cells through the chimeric receptor. Furthermore, tumor irradiation increased antigen-dressing onto DCs. In the absence of functional DCs, CAR T cell activity in irradiated tumor was short-lived and tumors relapsed. These findings establish a critical mechanism through which DCs maintain the CAR T cell pool in irradiated tumors, thus supporting translation of this approach to advance CAR T cell therapy for solid tumors.

immunology↗

Menin regulates androgen receptor- and MLL-driven condensation, upsetting regulation of cellular AR-driven transcription.

Menin is a protein that is regulated via protein-protein interactions by different binding partners, such as mixed lineage leukemia protein (MLL) and androgen receptor (AR). We observed that menin-AR and menin-MLL interactions are regulated by concentration-dependent dimerization of menin, and its interaction with cancer-related AR. As a result of its oligomerization-dependent interaction with both AR and MLL, menin is recruited into AR-RNA and MLL-RNA condensates formed by liquid-liquid phase separation (LLPS), with different outcomes under AR-overexpression or MLL-overexpression conditions representing different cancer types. At high concentrations promoting menin dimerization, it inhibits MLL-RNA LLPS, while making AR-RNA condensates less dynamic, i.e., more gel-like. Regions of AR show both negative/positive cooperativity in menin binding. AR contains a specific menin-binding region (MBR) in its intrinsically disordered N-terminal domain (NTD), menin binding of which is inhibited by the adjacent DNA-binding domain (DBD), but facilitated by a hinge region located between its DBD and ligand-binding domain (LBD) as well as by N terminus of AR. Interestingly, the hinge region reduces the propensity of full-length AR to undergo LLPS in the presence of RNA, which is facilitated by an alternative hinge region present in the tumor-specific AR isoform, AR-v7. As both menin and MLL are recruited into AR-driven, functional cellular condensates aggravated in the case of AR-v7, we posit that the menin-AR-MLL system represents a fine-tuned condensate module of transcription regulation that is balanced toward the tumor-suppressor activity of menin. Our results suggest that this balance can be upset by prevalent oncogenic events, such as menin upregulation and/or AR-v7 overexpression, in cancer.

biochemistry↗

Interdependence of a kinase and its cognate substrate plasma membrane nanoscale dynamics underlies Arabidopsis response to viral infection

Plant viruses represent a risk to agricultural production and as only a few treatments exist, it is urgent to identify resistance mechanisms and factors. In plant immunity, plasma membrane (PM)-localized proteins play an essential role in sensing the extracellular threat presented by bacteria, fungi or herbivores. Viruses are intracellular pathogens and as such the role of the plant PM in detection and resistance against viruses is often overlooked. We investigated the role of the partially PM-bound Calcium-dependent protein kinase 3 (CPK3) in viral infection and we discovered that it displayed a specific ability to hamper viral propagation over CPK isoforms that are involved in immune response to extracellular pathogens. More and more evidence support that the lateral organization of PM proteins and lipids underlies signal transduction in plants. We showed here that CPK3 diffusion in the PM is reduced upon activation as well as upon viral infection and that such immobilization depended on its substrate, Remorin (REM1.2), a scaffold protein. Furthermore, we discovered that the viral infection induced a CPK3-dependent increase of REM1.2 PM diffusion. Such interdependence was also observable regarding viral propagation. This study unveils a complex relationship between a kinase and its substrate that contrasts with the commonly described co-stabilisation upon activation while it proposes a PM-based mechanism involved in decreased sensitivity to viral infection in plants.

plant biology↗

Knowledge, attitudes and biosecurity practices among the small-scale dairy farmers in Sylhet District, Bangladesh

BackgroundIn the context of zoonosis, Bangladeshs small-scale dairying is yet to frame satisfactory levels due to poor biosecurity practices. ObjectivesThis study intended to reveal the degree of knowledge, attitudes, and biosecurity practices among Sylhet district, Bangladeshs small-scale dairy farmers. We also focused on the association between biosecurity practices and the incidence of non-specific enteritis in humans. MethodsA questionnaire-based survey was conducted on the farmers KAP via personal interviews of 15 farmers from the randomly selected fifteen small-scale dairy farms. The questionnaire was developed with six questions for knowledge, six questions for attitude, and 12 questions for the practice of biosecurity measures. Alongside that, data on the number of non-specific enteritis cases experienced by the farmers or their family members were also recorded. Spearman correlation was used to find out the correlation among KAP variables and between practice scores and non-specific enteritis incidences. ResultsWe found an insignificant (p > 0.05) influence of demographic characteristics over knowledge, attitude, and biosecurity practices. Significant (p<0.05) and strong correlations were found in knowledge-attitude (r = 0.65), knowledge-practice (r = 0.71), and attitude-practice (r = 0.64). Incidences of non-specific enteritis and biosecurity measures practice were also strongly correlated (r = -0.9232) and statistically significant (p<0.05). ConclusionsOur study suggests that increasing knowledge and developing a good attitude are necessary to increase the adaptation of biosecurity measures as three of these factors are correlated. Also, farm biosecurity measures are closely related to human health.

scientific communication and education↗

Application of polystyrene sulfonate (PSS) for inhibiting toxicity of ALS/FTD-linked dipeptide repeats

The GGGGCC (G4C2) expansion in the noncoding region of C9orf72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The repeat region is translated into five different dipeptide repeat proteins (DPRs), of which the arginine-rich DPRs (R-DPRs) poly- GR (GRn) and poly-PR (PRn) are highly neurotoxic. In this study, we characterized the protective effect against R- DPR toxicity of polystyrene sulfonate (PSS), an FDA-approved drug applied in hyperkalemia, in biochemical, cellular and iPSC-derived motor neuron (MN) models. We found that PSS, in a length-dependent manner, interacts very tightly with R-DPRs, and releases their bound RNA in R-DPR - RNA mixtures. PSS significantly influences the liquid- liquid phase separation (LLPS) of R-DPRs elicited by RNA and reduces their ensuing cell toxicity in Neuro-2a cells. PSS is cell penetrable, and it can effectively rescue the inhibitory effect R-DPRs on axonal mitochondrial transport in iPSC-derived MNs. Shorter (n < 340) variants of PSS are not toxic either to cells or to mice upon intracerebroventricular injection up to 1 mM concentration. Our results suggest that its polymeric nature endows PSS with an advantageous effect in C9-ALS providing a potential therapeutic tool against this debilitating neurodegenerative disease.

molecular biology↗

C9orf72-linked arginine-rich dipeptide repeats aggravate pathological phase separation of G3BP1

Ras GTPase-activating protein-binding protein 1 (G3BP1) is the key protein driving the formation of cytoplasmic stress granules (SGs) by liquid-liquid phase separation (LLPS). It is a switch-like protein held in a closed and inactive state by intramolecular electrostatic interactions competitively opened by RNA, activating the protein and initiating its LLPS. Here we show that C9orf72-derived arginine-rich dipeptide repeats PR30 and GR30 (R-DPRs) present in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), also bind to G3BP1, switching it to an LLPS-competent open state much more effectively than RNA. Whereas RNA binds G3BP1 with micromolar affinity, and cannot initiate LLPS without crowding agents, R-DPRs exhibit a thousand-fold stronger binding to G3BP1, eliciting rapid LLPS even without crowding. The pathogenic effect of R-DPRs is also underscored by the slow transition of R-DPR-G3BP1 liquid droplets to aggregated, ThS-positive states that can recruit the ALS-linked protein hnRNPA2. Deletion constructs and molecular simulations show that R-DPR binding and LLPS are mediated via binding through the negatively charged intrinsically disordered region 1 (IDR1) of the protein, allosterically regulated by the positively charged IDR3. Bioinformatic analyses point to the strong mechanistic parallels of these effects with the interaction of R-DPRs with nuclear nucleophosmin (NPM1) and also suggest that R-DPRs also interact with many other similar nucleolar and stress-granule proteins, extending the underlying mechanism of R-DPR toxicity in cells.

molecular biology↗

A mouse model of hormonal contraceptive exposure: depression, motivation, and the stress response

Hormonal contraceptives, including oral contraceptives (OCs), regulate hormonal cycles and broadly affect physiological processes, including stress responsivity. Whereas many users describe overall improved mood, up to 10% of OC users experience adverse effects, including depression and anxiety. Given the link between regulation of hypothalamic-pituitary-adrenal (HPA) axis, stress exposure, and risk for depression, it is likely that OC-effects on stress mediate increased risk or increased resilience to these disorders. In this study, we developed and characterized a tractable mouse model of OC exposure with which to identify the mechanisms underlying OC modulation of brain, behavior, and mood. Specifically, we aimed to determine whether translationally relevant doses of OC-hormones in mice mimic changes in stress responsivity observed in humans taking OCs and describe behavioral changes during OC exposure. Young adult female C57Bl/6N mice received daily ethinyl estradiol (EE) and levonorgestrel (LVNG) in 10% sucrose, EE and drospirenone (DRSP) in 10% sucrose, or 10% sucrose alone. Translationally relevant doses of EE+LVNG-exposure, but not EE+DRSP, suppressed the acute stress response, consistent with effects observed in human OC users. EE+LVNG caused a specific anhedonia-like effect, without broad changes in stress-coping behavior, other depression-like behaviors, or anxiety-like behaviors. The suppression of regular estrous cycling, together with the blunting of the corticosterone response to acute stress, demonstrate the utility of this model for future studies to identify the mechanisms underlying OC interactions with stress, motivation, and risk for depression.

neuroscience↗

A 2D Fragment-Assisted Protein Mimetic Approach to Rescue α-Synuclein Aggregation Mediated Early and Post-Disease Parkinsons Phenotypes

We have developed a Oligopyridylamide (OP) based 2-Dimensional Fragment-Assisted Structure-based Technique (2D-FAST) to identify potent antagonists of -Synuclein (S) aggregation, a process central to Parkinsons disease (PD). The 2D-FAST utilizes a fragment-based screening of large chemical space in OPs, which led to the identification of NS132 as an antagonist of the multiple facets of S aggregation. We also identified a better cell permeability analog (NS163) without sacrificing activity. OPs rescue S aggregation mediated PD phenotypes in muscle cells and dopaminergic (DA) neurons in C. elegans models. OPs prevent the progression of PD phenotypes in a novel post-disease onset PD model. This is one of the first examples of a synthetic mimetic-based 2D-FAST to identify antagonists of toxic S self-assembly. We envision that 2D-FAST will have tremendous potential as it is expandable for other oligoamide scaffolds and for a much larger chemical space to identify lead therapeutics for various diseases.

biochemistry↗

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↗

Prediction and Expression Analysis of Deleterious Nonsynonymous SNPs of Arabidopsis ACD11 Gene by Combining Computational Algorithms and Molecular Docking Approach

Accelerated cell death 11 (ACD11) is an autoimmune gene that suppresses pathogen infection in plants by preventing plant cells from becoming infected by any pathogen. This gene is widely known for growth inhibition, premature leaf chlorosis, and defense-related programmed cell death (PCD) in seedlings before flowering in Arabidopsis plant. Specific amino acid changes in the ACD11 proteins highly conserved domains are linked to autoimmune symptoms including constitutive defensive responses and necrosis without pathogen awareness. The molecular aspect of the aberrant activity of the ACD11 protein is difficult to ascertain. The purpose of our study was to find the most deleterious mutation position in the ACD11 protein and correlate them with their abnormal expression pattern. Using several computational methods, we discovered PCD vulnerable single nucleotide polymorphisms (SNPs) in ACD11. We analysed the RNA-Seq data, identified the detrimental nonsynonymous SNPs (nsSNP), built genetically mutated protein structures and used molecular docking to assess the impact of mutation. Our results demonstrated that the A15T and A39D variations in the GLTP domain were likely to be extremely detrimental mutations that inhibit the expression of the ACD11 protein domain by destabilizing its composition, as well as disrupt its catalytic effectiveness. When compared to the A15T mutant, the A39D mutant was more likely to destabilize the protein structure. In conclusion, these mutants can aid in the better understanding of the vast pool of PCD susceptibilities connected to ACD11 gene GLTP domain activation.

bioinformatics↗

Foldamers Reveal and Validate Novel Therapeutic Targets Associated with Toxic α-Synuclein Self-Assembly

Parkinsons disease (PD) is a progressive neurodegenerative disorder for which there is no successful prevention or intervention. The pathological hallmark for PD involves the self-assembly of functional Alpha-Synuclein (S) into non-functional amyloid structures. One of the potential therapeutic interventions against PD is the effective inhibition of S aggregation. However, the bottleneck towards achieving this goal is the identification of S domains/sequences that are essential for aggregation. Using a protein mimetic approach, we have identified S sequences-based novel targets that are essential for aggregation and will have significant therapeutic implications. An extensive array of in vitro, ex vivo, and in vivo assays was utilized to validate S sequences and their structural characteristics that are essential for aggregation and propagation of PD phenotypes. The study aids in developing significant mechanistic and therapeutic insights into various facets of S aggregation, which will pave the way for novel and effective treatments for PD.

biochemistry↗

Protein mimetic amyloid inhibitor potently abrogates cancer-associated mutant p53 aggregation and restores tumor suppressor function

Missense mutations in p53 are severely deleterious and occur in over 50% of all human cancers. The vast majority of these mutations are located in the inherently unstable DNA-binding domain (DBD), many of which destabilize the domain further and expose its aggregation-prone hydrophobic core, prompting self-assembly of mutant p53 into inactive cytosolic amyloid-like aggregates. Screening an oligopyridylamide library, previously shown to inhibit amyloid formation associated with Alzheimers disease and type II diabetes, identified a tripyridylamide, ADH-6, that potently abrogates self-assembly of the aggregation-nucleating subdomain of mutant p53 DBD. Moreover, ADH-6 effectively targets and dissociates mutant p53 aggregates in human cancer cells, which restores p53s transcriptional activity, leading to cell cycle arrest and apoptosis. Notably, ADH-6 treatment substantially shrinks xenografts harboring mutant p53 and prolongs survival, while exhibiting no toxicity to healthy tissue. This study demonstrates the first successful application of a bona fide small-molecule amyloid inhibitor as an anticancer agent.

cancer biology↗

In silico Identification and Functional Characterization of Conserved miRNAs in Fibre Biogenesis Crop Corchorus capsularis

Corchorus capsularis, commonly known as jute occupies the leading position in the production of natural fibre and fibre based products alongside lower environmental threat. Nowadays, the study of lignin biosynthesis pathways with other molecular basis of fibres formation are being more focused for its economic perspective. Small noncoding [~]21 to 24 nt nucleotides long microRNAs play significant roles in regulating the gene expression as well as different functions in cellular growth and development. Here, the study adopted a comprehensive in silico approach to identify and characterize the conserved miRNAs in the genome of C. capsularis including specific gene targets involved in the crucial cellular process. Expressed Sequence Tags (ESTs) based homology search of 3350 known miRNAs of dicotyledons were allowed against 763 non-redundant ESTs of jute genome resulted in the prediction of 5 potential miRNA candidates belonging five different miRNA families (miR1536, miR9567-3p, miR4391, miR11300, and miR8689). The putative miRNAs were 18 nucleotide length, within a range of -0.49 to -1.56 MFEI values and 55% to 61% of (A+U) content of their correspondence pre-miRNAs. A total of 1052 gene targets of putative miRNAs were identified and their functions were extensively analyzed. Most of the gene targets were involved in plant growth, cell cycle regulation, organelle synthesis, developmental process and environmental responses. The five gene targets, namely, NAC Domain Containing Protein, WRKY DNA binding protein, 3-dehydroquinate synthase, S-adenosyl-L-Met-dependent methyl transferase and Vascular-related NAC-Domain were found to be involved in the lignin biosynthesis, phenylpropanoid pathways and secondary wall formation which could play significant roles in the overall fibre biogenesis. The characterization of conserved miRNAs and their functional annotation of specific gene targets might enhance the more miRNA discovery, strengthening the complete understanding of miRNAs association in the cellular basis of lignin biosynthesis towards the production of high standard jute products.

genomics↗

Phylogeny and distinct properties of major intrinsic proteins in the genomes of six Phytophthora species suggest their novel functions in Phytophthora

ABSTRACTMajor intrinsic proteins (MIPs), commonly known as aquaporins, facilitate the membrane diffusion of water and some other non- polar solutes. MIPs might be involved in host-pathogen interactions. Herein, we identified 17, 24, 27, 19, 19, and 22 full-length MIPs, respectively, in the genomes of six Phytophthora species, P. infestans, P. parasitica, P. sojae, P. ramorum, P. capsici, and P. cinnamomi. These Phytophthora species are devastating plant pathogens and members of oomycetes, a distinct lineage of fungus-like eukaryotic microbes. Phylogenetic analysis showed that the Phytophthora MIPs (PMIPs) formed a completely distinct clade from their counterparts in other taxa and were clustered into nine subgroups. Sequence and structural properties indicated that the primary selectivity-related constrictions, including aromatic arginine (ar/R) selectivity filter and Froger’s positions in PMIPs were distinct from those in other taxa. The substitutions in the conserved Asn-Pro-Ala motifs in loops B and E of many PMIPs were also divergent from those in plants. We further deciphered group-specific consensus sequences/motifs in different loops and transmembrane helices of PMIPs, which were distinct from those in plants, animals, and microbes. The data collectively supported the notion that PMIPs might have novel functions.Competing Interest StatementThe authors have declared no competing interest.View Full Text

bioinformatics↗