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

Meiotic Crossover Patterning in Drosophila melanogaster

Meiosis is an essential process to halve an organism’s genome in preparation for transmission to the next generation. Recombination between homologous chromosomes is necessary for the proper segregation of chromosomes, and allows the generation of genetic diversity. Mistakes in meiosis can lead to aneuploidy, therefore, to minimize mistakes, recombination is a highly regulated process. Crossovers are patterned along a chromosome, and this patterning is dictated by three phenomena known as interference, assurance, and the centromere effect. Interference assures that a crossover does not occur too close to another crossover, assurance maintains that each chromosome gets at least one crossover, and the centromere effect suppresses crossovers that occur too close to the centromere. The work detailed in this dissertation first focuses on the proteins involved in crossover formation and then investigates the regulation of the suppression of centromere-proximal crossovers. I have gained insight into a potential endonuclease, Ankle1, as well as further elucidated the role of the mei-MCM complex in creating meiotic crossovers. In addition, I discovered that centromere-proximal crossover suppression is regulated both by the highly-repetitive heterochromatin adjacent to the centromere, as well as the protein-mediated centromere effect, which extends into the euchromatin and dissipates with distance from the centromere. Overall these findings have provided insight into the mechanisms of crossover formation and patterning and provided the foundation for future studies of meiotic crossover control.Doctor of Philosoph

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

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

ABSTRACT 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

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