Female meiosis and embryonic mitosis in Drosophila melanogaster

Dåvring, Lars; Sunner, Margareta

doi:10.1111/j.1601-5223.1973.tb01067.x

Cited by 45 publications

(6 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As noted above, in stages 9–10, the karyosome expands to the point that individual chromosomes can be detected [22–24]. These chromosomes recondense into a compact karyosome during stages 11–12, the exact time at which a reduction in the level of Mtrm causes precocious NEB.…”

Section: Resultsmentioning

confidence: 99%

The Inhibition of Polo Kinase by Matrimony Maintains G2 Arrest in the Meiotic Cell Cycle

et al. 2007

View full text Add to dashboard Cite

Many meiotic systems in female animals include a lengthy arrest in G2 that separates the end of pachytene from nuclear envelope breakdown (NEB). However, the mechanisms by which a meiotic cell can arrest for long periods of time (decades in human females) have remained a mystery. The Drosophila Matrimony (Mtrm) protein is expressed from the end of pachytene until the completion of meiosis I. Loss-of-function mtrm mutants result in precocious NEB. Coimmunoprecipitation experiments reveal that Mtrm physically interacts with Polo kinase (Polo) in vivo, and multidimensional protein identification technology mass spectrometry analysis reveals that Mtrm binds to Polo with an approximate stoichiometry of 1:1. Mutation of a Polo-Box Domain (PBD) binding site in Mtrm ablates the function of Mtrm and the physical interaction of Mtrm with Polo. The meiotic defects observed in mtrm/+ heterozygotes are fully suppressed by reducing the dose of polo+, demonstrating that Mtrm acts as an inhibitor of Polo. Mtrm acts as a negative regulator of Polo during the later stages of G2 arrest. Indeed, both the repression of Polo expression until stage 11 and the inactivation of newly synthesized Polo by Mtrm until stage 13 play critical roles in maintaining and properly terminating G2 arrest. Our data suggest a model in which the eventual activation of Cdc25 by an excess of Polo at stage 13 triggers NEB and entry into prometaphase.

show abstract

Section: Resultsmentioning

confidence: 99%

The Inhibition of Polo Kinase by Matrimony Maintains G2 Arrest in the Meiotic Cell Cycle

et al. 2007

View full text Add to dashboard Cite

show abstract

“…During these later stages a second potentially non-random competitive event occurs [ 94 – 96 ]. This latter process has been theorized to explain most transmission distortion [ 84 ].…”

Section: Drosophila As a Model For Studying Recombination Ramentioning

confidence: 99%

“…This latter process has been theorized to explain most transmission distortion [ 84 ]. During this time, only one in four gametes survives MII, becoming the pronucleus, while the rest become polar bodies [ 96 ]. If selection of the pronucleus is not random with respect to recombination, apparent differences in recombination rate may be observed.…”

Section: Drosophila As a Model For Studying Recombination Ramentioning

confidence: 99%

Recombination rate plasticity: revealing mechanisms by design

Stevison

Sefick

Rushton

et al. 2017

Phil. Trans. R. Soc. B

View full text Add to dashboard Cite

For over a century, scientists have known that meiotic recombination rates can vary considerably among individuals, and that environmental conditions can modify recombination rates relative to the background. A variety of external and intrinsic factors such as temperature, age, sex and starvation can elicit ‘plastic’ responses in recombination rate. The influence of recombination rate plasticity on genetic diversity of the next generation has interesting and important implications for how populations evolve. Further, many questions remain regarding the mechanisms and molecular processes that contribute to recombination rate plasticity. Here, we review 100 years of experimental work on recombination rate plasticity conducted in Drosophila melanogaster. We categorize this work into four major classes of experimental designs, which we describe via classic studies in D. melanogaster. Based on these studies, we highlight molecular mechanisms that are supported by experimental results and relate these findings to studies in other systems. We synthesize lessons learned from this model system into experimental guidelines for using recent advances in genotyping technologies, to study recombination rate plasticity in non-model organisms. Specifically, we recommend (1) using fine-scale genome-wide markers, (2) collecting time-course data, (3) including crossover distribution measurements, and (4) using mixed effects models to analyse results. To illustrate this approach, we present an application adhering to these guidelines from empirical work we conducted in Drosophila pseudoobscura.This article is part of the themed issue ‘Evolutionary causes and consequences of recombination rate variation in sexual organisms’.

show abstract

“…Therefore, oocytes at various stages of meiosis can be identified along the length of the ovariole. For example, zygotene‐stage germ cells are found in the germarium and in egg chambers of stage 1, while pachytene cells are found in stage 5 egg chambers [Davring and Sunner, ]. This greatly facilitates the study of meiotic progression, as ovarioles can be dissected and stained for mRNA or proteins of interest revealing the kinetics of expression of these factors during meiosis.…”

Section: Introductionmentioning

confidence: 99%

Models of germ cell development and their application for toxicity studies

Ferreira

Allard

2015

Environ and Mol Mutagen

View full text Add to dashboard Cite

Germ cells are unique in their ability to transfer genetic information and traits from generation to generation. As such, the proper development of germ cells and the integrity of their genome are paramount to the health of organisms and the survival of species. Germ cells are also exquisitely sensitive to environmental influences although the testing of germ cell toxicity, especially in females, has proven particularly challenging. In this review, we first describe the remarkable odyssey of germ cells in mammals, with an emphasis on the female germline, from their initial specification during embryogenesis to the generation of mature gametes in adults. We also describe the current methods used in germ cell toxicity testing and their limitations in examining the complex features of mammalian germ cell development. To bypass these challenges, we propose the use of alternative model systems such as Saccharomyces cerevisiae, Drosophila melanogaster, Caenorhabditis elegans and in vitro germ cell methods that have distinct advantages over traditional toxicity models. We discuss the benefits and limitations of each approach, their application to germ cell toxicity studies, and the need for computational approaches to maximize the usefulness of these models. Together, the inclusion of these alternative germ cell toxicity models will be invaluable for the examination of stages not easily accessible in mammals as well as the large scale, high-throughput investigation of germ cell toxicity.

show abstract

Female meiosis and embryonic mitosis in Drosophila melanogaster

Cited by 45 publications

References 11 publications

The Inhibition of Polo Kinase by Matrimony Maintains G2 Arrest in the Meiotic Cell Cycle

The Inhibition of Polo Kinase by Matrimony Maintains G2 Arrest in the Meiotic Cell Cycle

Recombination rate plasticity: revealing mechanisms by design

Models of germ cell development and their application for toxicity studies

Contact Info

Product

Resources

About