Using STEM Camps to Improve Female Interest in Technology Careers

Science, technology, engineering, and math (STEM) fields have been traditionally entered by men, often establishing women as underrepresented in many of these fields. This research study focuses on participants at a STEM camp for middle- and high-school girls designed to introduce them to technology. The camp was held 4 times over 3 years, with many of the participants from rural areas, underrepresented by race and economic status. Sixty camp attendees completed pre- and post-camp surveys and are referred to as the intervention group. A control group of 200 middle- and high-school girls who did not attend the camp also took the survey. This paper focuses on a subset of the survey results that sought to determine the impact on camp participants in the areas of technology self-efficacy and technology career interest as it related to management information systems (MIS). Analysis of the data collected found a significant difference in MIS self-efficacy between the intervention group and control group but no significant difference in choices of MIS-related careers. Results also include recommended improvements to STEM camp design

p53 protects against genome instability following centriole duplication failure

Centriole function has been difficult to study because of a lack of specific tools that allow persistent and reversible centriole depletion. Here we combined gene targeting with an auxin-inducible degradation system to achieve rapid, titratable, and reversible control of Polo-like kinase 4 (Plk4), a master regulator of centriole biogenesis. Depletion of Plk4 led to a failure of centriole duplication that produced an irreversible cell cycle arrest within a few divisions. This arrest was not a result of a prolonged mitosis, chromosome segregation errors, or cytokinesis failure. Depleting p53 allowed cells that fail centriole duplication to proliferate indefinitely. Washout of auxin and restoration of endogenous Plk4 levels in cells that lack centrioles led to the penetrant formation of de novo centrioles that gained the ability to organize microtubules and duplicate. In summary, we uncover a p53-dependent surveillance mechanism that protects against genome instability by preventing cell growth after centriole duplication failure

A USP28-53BP1-p53-p21 signaling axis arrests growth after centrosome loss or prolonged mitosis

Precise regulation of centrosome number is critical for accurate chromosome segregation and the maintenance of genomic integrity. In nontransformed cells, centrosome loss triggers a p53-dependent surveillance pathway that protects against genome instability by blocking cell growth. However, the mechanism by which p53 is activated in response to centrosome loss remains unknown. Here, we have used genome-wide CRISPR/Cas9 knockout screens to identify a USP28-53BP1-p53-p21 signaling axis at the core of the centrosome surveillance pathway. We show that USP28 and 53BP1 act to stabilize p53 after centrosome loss and demonstrate this function to be independent of their previously characterized role in the DNA damage response. Surprisingly, the USP28-53BP1-p53-p21 signaling pathway is also required to arrest cell growth after a prolonged prometaphase. We therefore propose that centrosome loss or a prolonged mitosis activate a common signaling pathway that acts to prevent the growth of cells that have an increased propensity for mitotic errors