CAP Profiles

Bio

Academic Appointments

Boards, Advisory Committees, Professional Organizations

  • Member, European Association for Cancer Research (EACR) (2012 - 2017)
  • Member, British Association for Cancer Research (BACR) (2012 - 2017)
  • Associate member, American Association for Cancer Research (AACR) (2012 - Present)
  • Communication officer, Stanford University Postdoctoral Association (SURPAS) (2015 - 2017)
  • Postdoctoral member, American Society for Cell Biology (ASCB) (2015 - Present)
  • Member, ASCB Committee for Postdocs and Students (COMPASS) (2017 - Present)

Contact

Research & Scholarship

Current Research and Scholarly Interests

I am a cell and molecular biologist by training. During my PhD I worked on the identification of thymidine kinase 1 phosphorylation status during cell cycle progression and its relevance for PET imaging of cell proliferation. In the Stearns lab I was interested in how cells cope with multiple centrosomes and what are the mechanisms ensuring centrosome number homeostasis. In the Sebastiano lab I am studying germ cell differentiation and what are the cell biological effects of de-differentiation.

Publications

All Publications

  • Growth disadvantage associated with centrosome amplification drives population-level centriole number homeostasis. Molecular biology of the cell Sala, R. n., Farrell, K. C., Stearns, T. n. 2020: mbcE19040195

    Abstract

    The centriole duplication cycle normally ensures that centriole number is maintained at two centrioles per G1 cell. However, some circumstances can result in an aberrant increase in centriole number-a phenotype that is particularly prevalent in several types of cancer. Following an artificial increase in centriole number without tetraploidization due to transient overexpression of the kinase PLK4, human cells return to a normal centriole number during the proliferation of the population. We examine the mechanisms responsible for this return to normal centriole number at the population level in human retinal pigment epithelial cells. We find that the return to normal centriole number in the population of induced cells cannot be explained by limited duplication of centrioles, instability of extra centrioles, or by grossly asymmetric segregation of extra centrioles in mitosis. However, cells with extra centrioles display heterogenous phenotypes including extended cell cycle arrest, longer interphase durations, and death, which overall result in a proliferative disadvantage relative to normal cells in the population. Although about half of cells with extra centrioles in a population were able to divide, the extent of the disadvantages conferred by other fates is sufficient to account for the observed rate of return to normal centriole number. These results suggest that only under conditions of either positive selection for cells with extra centrioles, continuous generation of such centrioles, or alleviation of the disadvantageous growth phenotypes, would they be maintained in a population.

    View details for DOI 10.1091/mbc.E19-04-0195

    View details for PubMedID 32966175

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