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Biology subjects

Karim, M. A.

Publications and source records attributed to Karim, M. A..

6 recordsLinked to original sources

Evaluation of Morpho-physiological Traits of F1 Hybrids and Estimation of Standard Heterosis of Sweet Pepper (Capsicum annuum L.) in Sylhet

Sweet pepper (Capsicum annuum L.) is a highly demanded crop valued for its culinary and nutritional benefits. This study aimed to evaluate the morphological, physiological, and yield-contributing traits of developed hybrids and check varieties, as well as estimate standard heterosis. The experiment was conducted at the Horticulture Department, Sylhet Agricultural University, from October 2022 to June 2023, using eight hybrids (P3xP1, P4xP3, P6xP5, P5xP1, P7xP1, P5xP3, P3xP2, and P6xP3) and two check varieties (CV1 and CV2). The field and laboratory experiments followed RCBD and CRD designs, respectively, with three replications. Significant morphological variations were observed in growth habit, leaf shape, flower position, fruit color, size, and nodal anthocyanin. The hybrids P5xP1, P7xP1, P6xP5, P3xP2, and P5xP3 exhibited superior morphological, physiological, and yield traits compared to check varieties. Earliness in flowering (30.33 days) and fruit setting (38.33 days) was recorded in P3xP1. Maximum fruit length (13.57 cm) was observed in P5xP1, while the highest fruit diameter (8.71 cm) and individual fruit weight (214.51 g) were found in P3xP2. The highest fruit yield per plant (1.94 kg) and per hectare (61.98 kg) was recorded in P5xP1. Positive standard heterosis was observed for key traits over check variety and mostly developed hybrids showed better performance in all traits compared to check variety. Pearson correlation and PCA analysis revealed key trait associations and genetic variation among sweet pepper hybrids, aiding breeding strategies. Considering morphological, physiological, yield potential and heterosis, P5xP1, P7xP1, P6xP5, P3xP2, and P5xP3 are recommended for further evaluation and breeding programs.

plant biology↗

A community driven GWAS summary statistics standard

Summary statistics from genome-wide association studies (GWAS) represent a huge potential for research. A challenge for researchers in this field is the access and sharing of summary statistics data due to a lack of standards for the data content and file format. For this reason, the GWAS Catalog hosted a series of meetings in 2021 with summary statistics stakeholders to guide the development of a standard format. The key requirements from the stakeholders were for a standard that contained key data elements to be able to support a wide range of data analyses, required low bioinformatics skills for file access and generation, to have easily accessible metadata, and unambiguous and interoperable data. Here, we define the specifications for the first version of the GWAS-SSF format, which was developed to meet the requirements discussed with the community. GWAS-SSF consists of a tab-separated data file with well-defined fields and an accompanying metadata file.

bioinformatics↗

Open Targets Genetics: An open approach to systematically prioritize causal variants and genes at all published GWAS trait-associated loci

Genome-wide association studies (GWAS) have identified many variants robustly associated with complex traits but identifying the gene(s) mediating such associations is a major challenge. Here we present an open resource that provides systematic fine-mapping and protein-coding gene prioritization across 133,441 published human GWAS loci. We integrate diverse data sources, including genetics (from GWAS Catalog and UK Biobank) as well as transcriptomic, proteomic and epigenomic data across many tissues and cell types. We also provide systematic disease-disease and disease-molecular trait colocalization results across 92 cell types and tissues and identify 729 loci fine-mapped to a single coding causal variant and colocalized with a single gene. We trained a machine learning model using the fine mapped genetics and functional genomics data using 445 gold standard curated GWAS loci to distinguish causal genes from background genes at the same loci, outperforming a naive distance based model. Genes prioritized by our model are enriched for known approved drug targets (OR = 8.1, 95% CI: [5.7, 11.5]). These results will be regularly updated and are publicly available through a web portal, Open Targets Genetics (OTG, http://genetics.opentargets.org), enabling users to easily prioritize genes at disease-associated loci and assess their potential as drug targets.

genetics↗

Profile of Molecular Subtypes of Breast Cancer Among Bangladeshi Women - Audit of Initial Experience

BackgroundReceptor status and molecular subtyping of breast cancer are crucial for patient management. We present here our initial experience on the status of different molecular subtypes and clinicopathological characteristics of invasive breast carcinomas in Bangladeshi population especially in Chittagong zone.\n\nMaterials and methodsA total of 59 histopathologically confirmed cases of invasive ductal carcinoma were selected for this study. Fifteen out of 59 cases were reported as HER2 equivalent and could not be categorized into any subtype because of the lack of availability of fluorescence in situ hybridization. The remaining 44 cases were distributed into different molecular subtypes and then the clinicopathological characteristics were compared for each molecular subtype.\n\nResultsAge ranges from 24-70 years with a mean age of 43.95 years. Most of the patients were in 41-50 years age group. Among the 44 cases, most common subtype was HER2/neu amplification (13 cases, 29.55%). Luminal A, luminal B and basal like subtypes were 11 (25%), 10 (22.73%) and 10 (22.73%) respectively. The mean tumor size was 3.46 cm and the highest mean tumor size was in basal-like subtype (4.01cm). Twenty five out of 59 cases (42.37%) showed axillary lymph node metastasis. Lowest axillary lymph node metastasis was found in luminal A subtype (3/11=27.27%).\n\nConclusionHER2/neu amplification subtype was found to be more common in this region. Luminal A subtype was found to be more favorable in comparison to the other subtypes in terms of axillary lymph node metastasis.

pathology↗

The Na+(K+)/H+ exchanger Nhx1 controls multivesicular body-vacuolar lysosome fusion

Loss-of-function mutations in human endosomal Na+(K+)/H+ Exchangers (NHEs) NHE6 and NHE9 are implicated in neurological disorders including Christianson Syndrome, autism and attention deficit and hyperactivity disorder (ADHD). These mutations disrupt retention of surface receptors within neurons and glial cells by affecting their delivery to lysosomes for degradation. However, the molecular basis of how these endosomal NHEs control endocytic trafficking is unclear. Using Saccharomyces cerevisiae as a model, we conducted cell-free organelle fusion assays to show that transport activity of the orthologous endosomal NHE Nhx1 is important for multivesicular body (MVB)-vacuolar lysosome fusion, the last step of endocytosis required for surface protein degradation. We find that deleting Nhx1 disrupts the fusogenicity of the MVB, not vacuole, by targeting pH-sensitive machinery downstream of the Rab-GTPase Ypt7 needed for SNARE-mediated lipid bilayer merger. All contributing mechanisms are evolutionarily conserved offering new insight into the etiology of human disorders linked to loss of endosomal NHE function.

cell biology↗

Distinct features of multivesicular body-lysosome fusion revealed by a new cell-free content-mixing assay

When marked for degradation, surface receptor and transporter proteins are internalized and delivered to endosomes where they are packaged into intralumenal vesicles (ILVs). Many rounds of ILV formation create multivesicular bodies (MVBs) that fuse with lysosomes exposing ILVs to hydrolases for catabolism. Despite being critical for protein degradation, the molecular underpinnings of MVB-lysosome fusion remain unclear, although machinery underlying other lysosome fusion events is implicated. But how then is specificity conferred? And how is MVB maturation and fusion coordinated for efficient protein degradation? To address these questions, we developed a cell-free MVB-lysosome fusion assay using S. cerevisiae as a model. After confirming that the Rab7 ortholog Ypt7 and the multisubunit tethering complex HOPS are required, we found that the Qa-SNARE Pep12 distinguishes this event from homotypic lysosome fusion. Mutations that impair MVB maturation block fusion by preventing Ypt7 activation, confirming that a Rab-cascade mechanism harmonizes MVB maturation with lysosome fusion.\n\nIMPACT STATEMENTEndocytosis culminates with multivesicular bodies (MVBs) fusing with lysosomes. But the molecular underpinnings of this event remain unclear. Here, using S. cerevisiae as a model, Karim et al. employ a new in vitro assay to show that MVB-lysosome fusion is driven by ESCRT-dependent Rab-GTPase activation and the syntaxin ortholog Pep12, distinguishing it from other lysosome membrane fusion events.

cell biology↗