Practical lab exercises that help students draw connections between genotype and phenotype, and make and test predictions about the identity of mutants, are invaluable in college-level cell biology, genetics, and microbiology courses. While many bacteria are easy to grow and manipulate within the time and resource constraints of a laboratory course, their phenotypes are not always observable or relevant-seeming to college students. Here, we leverage sporulation by the bacterium Bacillus subtilis, a well-characterized and genetically tractable system, to create 5 adaptable lab exercises that can be implemented in different combinations to suit the needs of a variety of courses and instruction modes. Because phenotypic changes during sporulation are striking morphological changes to cells that are easily observable with basic light microscopy, and because spore-forming bacteria related to B. subtilis have clear applications for human and environmental health, these exercises have the potential to engage students' interest while introducing and reinforcing key concepts in microbiology, cell biology, and genetics.
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http://dx.doi.org/10.1128/jmbe.00149-21 | DOI Listing |
PLoS One
January 2025
INRAE, Biologie du Fruit et Pathologie, Université de Bordeaux, UMR 1332, Villenave d'Ornon, France.
Rain cracking compromises quality and quantity of sweet cherries worldwide. Cracking susceptibility differs among genotypes. The objective was to (1) phenotype the progeny of a cross between a tolerant and a susceptible sweet cherry cultivar for cuticle mass per unit area, strain release on cuticle isolation, cuticular microcracking and calcium/dry mass ratio and (2) relate these characteristics to cracking susceptibilities evaluated in laboratory immersion assays and published multiyear field observations.
View Article and Find Full Text PDFJ Clin Immunol
January 2025
Division of Allergy and Immunology, Children's Hospital of Philadelphia, Philadelphia, 19104, USA.
Major histocompatibility complex class I deficiency results from deleterious biallelic variants in TAP1, TAP2, TAPBP, and B2M genes. Only a few patients with variant-curated TAP1 deficiency (TAP1D) have been reported in the literature and the clinical phenotype has been variable with an emphasis on autoimmune and inflammatory complications. We report TAP1D in a Nepalese girl with a severe clinical phenotype with serious viral infections at a very young age.
View Article and Find Full Text PDFCalcif Tissue Int
January 2025
Department of Paediatric Endocrinology, Alder Hey Children's Hospital, Liverpool, UK.
Autosomal recessive hypophosphatemic rickets type 2 (ARHR2) is an uncommon hereditary form of rickets characterised by chronic renal phosphate loss and impaired bone mineralisation. This results from compound heterozygous or homozygous pathogenic variants in ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), a key producer of extracellular inorganic pyrophosphate (PPi) and an inhibitor of fibroblast growth factor23 (FGF23). ENPP1 deficiency impacts FGF23 and increases its activity.
View Article and Find Full Text PDFJ Neural Transm (Vienna)
January 2025
Neurology Department, LR18SP03, Razi University Hospital, Tunis, Tunisia.
Amyotrophic Lateral Sclerosis(ALS) has traditionally been managed as a neuromuscular disorder. However, recent evidence suggests involvement of non-motor domains. This study aims to evaluate the impact of APOE and MAPT genotypes on the cognitive features of ALS.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Washington University School of Medicine, Saint Louis, MO, USA.
Background: The recent European-ancestry based genome-wide association study (GWAS) of Alzheimer disease (AD) by Bellenguez2022 has identified 75 significant genetic loci, but only a few have been functionally mapped to effector gene level. Besides the large-scale RNA expression, protein and metabolite levels are key molecular traits bridging the genetic variants to AD risk, and thus we decided to integrate them into the genetic analysis to pinpoint key proteins and metabolites underlying AD etiology. Few studies have generated more than one layer of post-transcriptional phenotypes, limiting the scale of biological translation of disease modifying treatments.
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