Professional Education

  • Doctor of Philosophy, Johns Hopkins University (2021)
  • Bachelor of Science, Pennsylvania State University (2013)
  • Doctor of Philosophy, Johns Hopkins Bloomberg School of Public Health, Regulation of the G2/MI transition by Aurora and Polo-like kinases during mammalian spermatogenesis (2021)
  • Bachelor of Sciences, Pennsylvania State University, Biochemistry and Molecular Biology (2013)

Stanford Advisors

All Publications

  • Meiotic recombination mirrors patterns of germline replication in mice and humans CELL Pratto, F., Brick, K., Cheng, G., Lam, K., Cloutier, J. M., Dahiya, D., Wellard, S. R., Jordan, P. W., Camerini-Otero, R. 2021; 184 (16): 4251-+


    Genetic recombination generates novel trait combinations, and understanding how recombination is distributed across the genome is key to modern genetics. The PRDM9 protein defines recombination hotspots; however, megabase-scale recombination patterning is independent of PRDM9. The single round of DNA replication, which precedes recombination in meiosis, may establish these patterns; therefore, we devised an approach to study meiotic replication that includes robust and sensitive mapping of replication origins. We find that meiotic DNA replication is distinct; reduced origin firing slows replication in meiosis, and a distinctive replication pattern in human males underlies the subtelomeric increase in recombination. We detected a robust correlation between replication and both contemporary and historical recombination and found that replication origin density coupled with chromosome size determines the recombination potential of individual chromosomes. Our findings and methods have implications for understanding the mechanisms underlying DNA replication, genetic recombination, and the landscape of mammalian germline variation.

    View details for DOI 10.1016/j.cell.2021.06.025

    View details for Web of Science ID 000682521800012

    View details for PubMedID 34260899

  • Overlapping roles for PLK1 and Aurora A during meiotic centrosome biogenesis in mouse spermatocytes EMBO REPORTS Wellard, S. R., Zhang, Y., Shults, C., Zhao, X., McKay, M., Murray, S. A., Jordan, P. W. 2021; 22 (4): e51023


    The establishment of bipolar spindles during meiotic divisions ensures faithful chromosome segregation to prevent gamete aneuploidy. We analyzed centriole duplication, as well as centrosome maturation and separation during meiosis I and II using mouse spermatocytes. The first round of centriole duplication occurs during early prophase I, and then, centrosomes mature and begin to separate by the end of prophase I to prime formation of bipolar metaphase I spindles. The second round of centriole duplication occurs at late anaphase I, and subsequently, centrosome separation coordinates bipolar segregation of sister chromatids during meiosis II. Using a germ cell-specific conditional knockout strategy, we show that Polo-like kinase 1 and Aurora A kinase are required for centrosome maturation and separation prior to metaphase I, leading to the formation of bipolar metaphase I spindles. Furthermore, we show that PLK1 is required to block the second round of centriole duplication and maturation until anaphase I. Our findings emphasize the importance of maintaining strict spatiotemporal control of cell cycle kinases during meiosis to ensure proficient centrosome biogenesis and, thus, accurate chromosome segregation during spermatogenesis.

    View details for DOI 10.15252/embr.202051023

    View details for Web of Science ID 000620216500001

    View details for PubMedID 33615678

    View details for PubMedCentralID PMC8024899

  • Aurora B and C kinases regulate chromosome desynapsis and segregation during mouse and human spermatogenesis JOURNAL OF CELL SCIENCE Wellard, S. R., Schindler, K., Jordan, P. W. 2020; 133 (23)

    View details for DOI 10.1242/jcs.248831

    View details for Web of Science ID 000599515200007

  • A Seminiferous Tubule Squash Technique for the Cytological Analysis of Spermatogenesis Using the Mouse Model JOVE-JOURNAL OF VISUALIZED EXPERIMENTS Wellard, S. R., Hopkins, J., Jordan, P. W. 2018


    Meiotic progression in males is a process that requires the concerted action of a number of highly regulated cellular events. Errors occurring during meiosis can lead to infertility, pregnancy loss or genetic defects. Commencing at the onset of puberty and continuing throughout adulthood, continuous semi-synchronous waves of spermatocytes undergo spermatogenesis and ultimately form haploid sperm. The first wave of mouse spermatocytes undergoing meiotic initiation appear at day 10 post-partum (10 dpp) and are released into the lumen of seminiferous tubules as mature sperm at 35 dpp. Therefore, it is advantageous to utilize mice within this developmental time-window in order to obtain highly enriched populations of interest. Analysis of rare cell stages is more difficult in older mice due to the contribution of successive spermatogenic waves, which increase the diversity of the cellular populations within the tubules. The method described here is an easily implemented technique for the cytological evaluation of the cells found within the seminiferous tubules of mice, including spermatogonia, spermatocytes, and spermatids. The tubule squash technique maintains the integrity of isolated male germ cells and allows examination of cellular structures that are not easily visualized with other techniques. To demonstrate the possible applications of this tubule squash technique, spindle assembly was monitored in spermatocytes progressing through the prophase to metaphase I transition (G2/MI transition). In addition, centrosome duplication, meiotic sex chromosome inactivation (MSCI), and chromosome bouquet formation were assessed as examples of the cytological structures that can be observed using this tubule squash method. This technique can be used to pinpoint specific defects during spermatogenesis that are caused by mutation or exogenous perturbation, and thus, contributes to our molecular understanding of spermatogenesis.

    View details for DOI 10.3791/56453

    View details for Web of Science ID 000426453400019

    View details for PubMedID 29443055

    View details for PubMedCentralID PMC5912363