Search for: All records

Mastery of quantitative skills is increasingly critical for student success in life sciences, but few curricula adequately incorporate quantitative skills. Quantitative Biology at Community Colleges (QB@CC) is designed to address this need by building a grassroots consortium of community college faculty to 1) engage in interdisciplinary partnerships that increase participant confidence in life science, mathematics, and statistics domains; 2) generate and publish a collection of quantitative skills–focused open education resources (OER); and 3) disseminate these OER and pedagogical practices widely, in turn expanding the network. Currently in its third year, QB@CC has recruited 70 faculty into the network and created 20 modules. Modules can be accessed by interested biology and mathematics educators in high school, 2-year, and 4-year institutions. Here, we use survey responses, focus group interviews, and document analyses (principles-focused evaluation) to evaluate the progress in accomplishing these goals midway through the QB@CC program. The QB@CC network provides a model for developing and sustaining an interdisciplinary community that benefits participants and generates valuable resources for the broader community. Similar network-building programs may wish to adopt some of the effective aspects of the QB@CC network model to meet their objectives. 

Abstract The fungus Magnaporthe oryzae causes devastating diseases of crops, including rice and wheat, and in various grasses. Strains from ryegrasses have highly unstable chromosome ends that undergo frequent rearrangements, and this has been associated with the presence of retrotransposons (Magnaporthe oryzae Telomeric Retrotransposons—MoTeRs) inserted in the telomeres. The objective of the present study was to determine the mechanisms by which MoTeRs promote telomere instability. Targeted cloning, mapping, and sequencing of parental and novel telomeric restriction fragments (TRFs), along with MinION sequencing of genomic DNA allowed us to document the precise molecular alterations underlying 109 newly-formed TRFs. These included truncations of subterminal rDNA sequences; acquisition of MoTeR insertions by ‘plain’ telomeres; insertion of the MAGGY retrotransposons into MoTeR arrays; MoTeR-independent expansion and contraction of subtelomeric tandem repeats; and a variety of rearrangements initiated through breaks in interstitial telomere tracts that are generated during MoTeR integration. Overall, we estimate that alterations occurred in approximately sixty percent of chromosomes (one in three telomeres) analyzed. Most importantly, we describe an entirely new mechanism by which transposons can promote genomic alterations at exceptionally high frequencies, and in a manner that can promote genome evolution while minimizing collateral damage to overall chromosome architecture and function.