Developing Scientific Communication Skills Using Primary Literature in an Undergraduate Cell Biology Course.

Being able to communicate scientifically is an important skill for students graduating with a science degree. Skills used in future graduate school and careers for science majors include oral and written communication, as well as science literacy and being able to create figures to display information. There is a consensus that these skills should be taught throughout an undergraduate science curriculum; however, many instructors have cited insufficient time to cover skills and develop materials to effectively incorporate these skills, especially into lower-level content-focused courses. Here, we present an active curriculum that can easily be incorporated into any content-focused undergraduate Cell Biology course. The curriculum is designed around scientific literature that engages students in a multitude of active learning activities to develop different types of scientific communication skills. This curriculum not only develops student skills and self-efficacy in scientific communication, it also engages them in course content and stimulates their interest in research. While making changes to a course to include scientific communication can be difficult, making small changes, such as addition of this curriculum to an already-existing content-focused course, could make a big difference in the skills and attitudes of early undergraduate science students.

Centromere-Proximal Meiotic Crossovers in Drosophila melanogaster Are Suppressed by Both Highly Repetitive Heterochromatin and Proximity to the Centromere.

Crossovers are essential in meiosis of most organisms to ensure the proper segregation of chromosomes, but improper placement of crossovers can result in nondisjunction and aneuploidy in progeny. In particular, crossovers near the centromere can cause nondisjunction. Centromere-proximal crossovers are suppressed by what is termed the centromere effect, but the mechanism is unknown. Here, we investigate contributions to centromere-proximal crossover suppression in Drosophila melanogaster We mapped a large number of centromere-proximal crossovers, and find that crossovers are essentially absent from the highly repetitive (HR)-heterochromatin surrounding the centromere but occur at a low frequency within the less-repetitive (LR)-heterochromatic region and adjacent euchromatin. Previous research suggested that flies that lack the Bloom syndrome helicase (Blm) lose meiotic crossover patterning, including the centromere effect. Mapping of centromere-proximal crossovers in Blm mutants reveals that the suppression within the HR-heterochromatin is intact, but the distance-dependent centromere effect is lost. We conclude that centromere-proximal crossovers are suppressed by two separable mechanisms: an HR-heterochromatin effect that completely suppresses crossovers in the HR-heterochromatin, and the centromere effect, which suppresses crossovers with a dissipating effect with distance from the centromere.

Meiotic MCM Proteins Promote and Inhibit Crossovers During Meiotic Recombination.

Crossover formation as a result of meiotic recombination is vital for the proper segregation of homologous chromosomes at the end of meiosis I. In many organisms, crossovers are generated through two crossover pathways: Class I and Class II. To ensure accurate crossover formation, meiosis-specific protein complexes regulate the degree to which each pathway is used. One such complex is the mei-mini-chromosome maintenance (MCM) complex, which contains MCM and MCM-like proteins REC (ortholog of Mcm8), MEI-217, and MEI-218. The mei-MCM complex genetically promotes Class I crossovers and inhibits Class II crossovers in Drosophila, but it is unclear how individual mei-MCM proteins contribute to crossover regulation. In this study, we perform genetic analyses to understand how specific regions and motifs of mei-MCM proteins contribute to Class I and II crossover formation, and distribution. Our analyses show that the long, disordered N-terminus of MEI-218 is dispensable for crossover formation, and that mutations that disrupt REC's Walker A and B motifs differentially affect Class I and Class II crossover formation. In rec Walker A mutants, Class I crossovers exhibit no change but Class II crossovers are increased. However, in rec Walker B mutants, Class I crossovers are severely impaired and Class II crossovers are increased. These results suggest that REC may form multiple complexes that exhibit differential REC-dependent ATP-binding and -hydrolyzing requirements. These results provide genetic insight into the mechanisms through which mei-MCM proteins promote Class I crossovers and inhibit Class II crossovers.

The absence of crossovers on chromosome 4 in Drosophila melanogaster: Imperfection or interesting exception?

Drosophila melanogaster chromosome 4 is an anomaly because of its small size, chromatin structure, and most notably its lack of crossing over during meiosis. Earlier ideas about the absence of crossovers on 4 hypothesize that these unique characteristics function to prevent crossovers. Here, we explore hypotheses about the absence of crossovers on 4, how these have been addressed, and new insights into the mechanism behind this suppression. We review recently published results that indicate that global crossover patterning, in particular the centromere effect, make a major contribution to the prevention of crossovers on 4.

Bloom Syndrome Helicase Promotes Meiotic Crossover Patterning and Homolog Disjunction.

In most sexually reproducing organisms, crossover formation between homologous chromosomes is necessary for proper chromosome disjunction during meiosis I. During meiotic recombination, a subset of programmed DNA double-strand breaks (DSBs) are repaired as crossovers, with the remainder becoming noncrossovers [1]. Whether a repair intermediate is designated to become a crossover is a highly regulated decision that integrates several crossover patterning processes, both along chromosome arms (interference and the centromere effect) and between chromosomes (crossover assurance) [2]. Because the mechanisms that generate crossover patterning have remained elusive for over a century, it has been difficult to assess the relationship between crossover patterning and meiotic chromosome behavior. We show here that meiotic crossover patterning is lost in Drosophila melanogaster mutants that lack the Bloom syndrome helicase. In the absence of interference and the centromere effect, crossovers are distributed more uniformly along chromosomes. Crossovers even occur on the small chromosome 4, which normally never has meiotic crossovers [3]. Regulated distribution of crossovers between chromosome pairs is also lost, resulting in an elevated frequency of homologs that do not receive a crossover, which in turn leads to elevated nondisjunction.