-
[
J Med Entomol,
1989]
Intracellular melanization responses to developing larvae of Brugia species (B. malayi (Buckley), B. pahangi (Buckley and Edeson), and B. patei (Buckley, Nelson, and Heisch] in the thoracic muscle fibers of eight strains of Anopheles quadrimaculatus Say were first observed 48 to 72 h after an infective blood meal. Three to 4 d later, large numbers of melanized first-stage larvae were found within the thoracic muscle fibers. These intracellular responses were in addition to the extracellular responses to microfilariae and microfilarial sheaths of B. pahangi in the abdominal hemocoel of An. quadrimaculatus described in literature. Simultaneously, normal development of larvae of the three Brugia species also was observed in all eight strains of An. quadrimaculatus. Comparisons of melanized first-stage larvae and normally developing larvae of the three Brugia species in the thoracic muscle fibers of the eight strains of An. quadrimaculatus showed that there were distinct variations in numbers of melanized and developing larvae and percentage of females with melanized and developing larvae in different strains. Numbers of melanized first-stage larvae reflected the extent of refractoriness of An. quadrimaculatus strains. Fully melanized larvae showed no abnormalities in parasite organelles, indicating that refractoriness is due to an enhanced ability of the host to recognize the living parasite. Further comparison among the strains suggested that the mutants, Yellow Larvae and Vero Beach Colony were significantly more susceptible, and Red Stripe was the most refractory to all three Brugia species. Thus, the gene(s) controlling susceptibility and refractoriness to all three Brugia species probably occurs on the same autosomal chromosome as the mutations in these strains. The significance of intracellular melanization of filarial larvae is discussed with reference to the melanization responses to different parasites in other mosquitoes.
-
[
PLoS Comput Biol,
2017]
Genetic diversity is maintained by continuing generation and removal of variants. While examining over 800,000 DNA variants in wild isolates of Caenorhabditis elegans, we made a discovery that the proportions of variant types are not constant across the C. elegans genome. The variant proportion is defined as the fraction of a specific variant type (e.g. single nucleotide polymorphism (SNP) or indel) within a broader set of variants (e.g. all variants or all non-SNPs). The proportions of most variant types show a correlation with the recombination rate. These correlations can be explained as a result of a concerted action of two mutation mechanisms, which we named Morgan and Sanger mechanisms. The two proposed mechanisms act according to the distinct components of recombination rate, specifically the genetic and physical distance. Regression analysis was used to explore the characteristics and contributions of the two mutation mechanisms. According to our model, ~20-40% of all mutations in C. elegans wild populations are derived from programmed meiotic double strand breaks, which precede chromosomal crossovers and thus may be the point of origin for the Morgan mechanism. A substantial part of the known correlation between the recombination rate and variant distribution appears to be caused by the mutations generated by the Morgan mechanism. Mathematically integrating the mutation model with background selection model gives a more complete depiction of how the variant landscape is shaped in C. elegans. Similar analysis should be possible in other species by examining the correlation between the recombination rate and variant landscape within the context of our mutation model.
-
[
Biochem Mol Biol Educ,
2006]
We describe an eight-week summer Young Scientist in Training (YSIT) internship program involving middle and high school students. This program exposed students to current basic research in molecular genetics, while introducing or reinforcing principles of the scientific method and demonstrating the uses of mathematics and chemistry in biology. For the laboratory-based program, selected students from Baltimore City Schools working in groups of three were teamed with undergraduate research assistants at Morgan State University. Teams were assigned a project that was indirectly related to our laboratory research on the characterization of gene expression in Caenorhabditis elegans. At the end of the program, teams prepared posters detailing their accomplishments, and presented their findings to parents and faculty members during a mini-symposium. The posters were also submitted to the respective schools and the interns were offered a presentation of their research at local high school science fairs.
-
[
Cell Biol Educ,
2003]
A 14-week, undergraduate-level Genetics and Population Biology course at Morgan State University was modified to include a demonstration of functional genomics in the research laboratory. Students performed a rudimentary sequence analysis of the Caenorhabditis elegans genome and further characterized three sequences that were predicted to encode helix-loop-helix proteins. Students then used reverse transcription-polymerase chain reaction to determine which of the three genes is normally expressed in C. elegans. At the end of this laboratory activity, students were 1) to demonstrate a rudimentary knowledge of bioinformatics, including the ability to differentiate between "having" a gene and "expressing" a gene, and 2) to understand basic approaches to functional genomics, including one specific technique for assaying for gene expression. It was also anticipated that students would increase their skills at effectively communicating their research activities through written and/or oral presentation. This article describes the laboratory activity and the assessment of the effectiveness of the activity.
-
[
Mol Genet Genomics,
2002]
Mutations in the Drosophila miniature-dusky ( m-dy) gene complex were first reported by Morgan and Bridges about 90 years ago. m-dy mutants have abnormally small wings, a phenotype attributed to a cell-autonomous reduction in the size of the epidermal cells comprising the differentiated wing. Using a molecular genetic approach, we have characterized the m-dy chromosomal interval and identified a pair of adjacent transcription units corresponding to m and dy. A dy mutant known as dy (And) has a single base substitution within the protein-coding region that is predicted to result in an amber stop codon and premature translational termination. We show that dy mRNA is expressed at two discrete periods during the life cycle - one during embryonic development and early larval instars, the second during adult development, coincident with wing differentiation. In agreement with the phenotypic similarity of m and dy mutants, sequence comparisons reveal a similarity between the predicted MINIATURE and DUSKY proteins, and indicate that the m and dy genes are members of a larger Drosophila gene family. Both m and dy, as well as other members of this superfamily, are predicted to encode transmembrane proteins with similarity to C. elegans cuticle proteins known as cuticulins. We postulate that m, dy and other members of this protein superfamily function as structural components of the Drosophila cuticulin layer. Such a role for m and dy products in wing differentiation is sufficient to explain the morphological phenotypes associated with m-dy mutants.