An evidence-based evaluation of transferrable skills and job satisfaction for science PhDs.

PhD recipients acquire discipline-specific knowledge and a range of relevant skills during their training in the life sciences, physical sciences, computational sciences, social sciences, and engineering. Empirically testing the applicability of these skills to various careers held by graduates will help assess the value of current training models. This report details results of an Internet survey of science PhDs (n = 8099) who provided ratings for fifteen transferrable skills. Indeed, analyses indicated that doctoral training develops these transferrable skills, crucial to success in a wide range of careers including research-intensive (RI) and non-research-intensive (NRI) careers. Notably, the vast majority of skills were transferrable across both RI and NRI careers, with the exception of three skills that favored RI careers (creativity/innovative thinking, career planning and awareness skills, and ability to work with people outside the organization) and three skills that favored NRI careers (time management, ability to learn quickly, ability to manage a project). High overall rankings suggested that graduate training imparted transferrable skills broadly. Nonetheless, we identified gaps between career skills needed and skills developed in PhD training that suggest potential areas for improvement in graduate training. Therefore, we suggest that a two-pronged approach is crucial to maximizing existing career opportunities for PhDs and developing a career-conscious training model: 1) encouraging trainees to recognize their existing individual skill sets, and 2) increasing resources and programmatic interventions at the institutional level to address skill gaps. Lastly, comparison of job satisfaction ratings between PhD-trained employees in both career categories indicated that those in NRI career paths were just as satisfied in their work as their RI counterparts. We conclude that PhD training prepares graduates for a broad range of satisfying careers, potentially more than trainees and program leaders currently appreciate.

Diversity Exiting the Academy: Influential Factors for the Career Choice of Well-Represented and Underrepresented Minority Scientists.

A national sample of PhD-trained scientists completed training, accepted subsequent employment in academic and nonacademic positions, and were queried about their previous graduate training and current employment. Respondents indicated factors contributing to their employment decision (e.g., working conditions, salary, job security). The data indicate the relative importance of deciding factors influencing career choice, controlling for gender, initial interest in faculty careers, and number of postgraduate publications. Among both well-represented (WR; n = 3444) and underrepresented minority (URM; n = 225) respondents, faculty career choice was positively associated with desire for autonomy and partner opportunity and negatively associated with desire for leadership opportunity. Differences between groups in reasons endorsed included: variety, prestige, salary, family influence, and faculty advisor influence. Furthermore, endorsement of faculty advisor or other mentor influence and family or peer influence were surprisingly rare across groups, suggesting that formal and informal support networks could provide a missed opportunity to provide support for trainees who want to stay in faculty career paths. Reasons requiring alteration of misperceptions (e.g., limited leadership opportunity for faculty) must be distinguished from reasons requiring removal of actual barriers. Further investigation into factors that affect PhDs' career decisions can help elucidate why URM candidates are disproportionately exiting the academy.

Preparing Postbaccalaureates for Entry and Success in Biomedical PhD Programs.

Certain racial and ethnic groups, individuals with disabilities, and those from low socioeconomic backgrounds remain underrepresented (UR) in the biomedical sciences. This underrepresentation becomes more extreme at each higher education stage. To support UR scholars during the critical transition from baccalaureate to PhD, we established an intensive, 1-yr postbaccalaureate training program. We hypothesized that this intervention would strengthen each participant's competitiveness for leading PhD programs and build a foundation of skills and self-efficacy important for success during and after graduate school. Scholar critical analysis skills, lab technique knowledge, and Graduate Record Examination scores all improved significantly during the program. Scholars reported significant confidence growth in 21 of 24 categories related to success in research careers. In 5 yr, 91% (41/45) of scholars transitioned directly into PhD programs. Importantly, 40% (18/45) of participating postbaccalaureate scholars had previously been declined acceptance into graduate school; however, 17/18 of these scholars directly entered competitive PhD programs following our training program. Alumni reported they were "extremely well" prepared for graduate school, and 95% (39/41) are currently making progress to graduation with a PhD. In conclusion, we report a model for postbaccalaureate training that could be replicated to increase participation and success among UR scholars in the biomedical sciences.

Internalization of multiple cells during C. elegans gastrulation depends on common cytoskeletal mechanisms but different cell polarity and cell fate regulators.

Understanding the links between developmental patterning mechanisms and force-producing cytoskeletal mechanisms is a central goal in studies of morphogenesis. Gastrulation is the first morphogenetic event in the development of many organisms. Gastrulation involves the internalization of surface cells, often driven by the contraction of actomyosin networks that are deployed with spatial precision-both in specific cells and in a polarized manner within each cell. These cytoskeletal mechanisms rely on different cell fate and cell polarity regulators in different organisms. Caenorhabditis elegans gastrulation presents an opportunity to examine the extent to which diverse mechanisms may be used by dozens of cells that are internalized at distinct times within a single organism. We identified 66 cells that are internalized in C. elegans gastrulation, many of which were not known previously to gastrulate. To gain mechanistic insights into how these cells internalize, we genetically manipulated cell fate, cell polarity and cytoskeletal regulators and determined the effects on cell internalization. We found that cells of distinct lineages depend on common actomyosin-based mechanisms to gastrulate, but different cell fate regulators, and, surprisingly, different cell polarity regulators. We conclude that diverse cell fate and cell polarity regulators control common mechanisms of morphogenesis in C. elegans. The results highlight the variety of developmental patterning mechanisms that can be associated with common cytoskeletal mechanisms in the morphogenesis of an animal embryo.

Apical constriction: a cell shape change that can drive morphogenesis.

Biologists have long recognized that dramatic bending of a cell sheet may be driven by even modest shrinking of the apical sides of cells. Cell shape changes and tissue movements like these are at the core of many of the morphogenetic movements that shape animal form during development, driving processes such as gastrulation, tube formation, and neurulation. The mechanisms of such cell shape changes must integrate developmental patterning information in order to spatially and temporally control force production-issues that touch on fundamental aspects of both cell and developmental biology and on birth defects research. How does developmental patterning regulate force-producing mechanisms, and what roles do such mechanisms play in development? Work on apical constriction from multiple systems including Drosophila, Caenorhabditis elegans, sea urchin, Xenopus, chick, and mouse has begun to illuminate these issues. Here, we review this effort to explore the diversity of mechanisms of apical constriction, the diversity of roles that apical constriction plays in development, and the common themes that emerge from comparing systems.

Multiple paxillin binding sites regulate FAK function.

BACKGROUND: FAK localization to focal adhesions is essential for its activation and function. Localization of FAK is mediated through the C-terminal focal adhesion targeting (FAT) domain. Recent structural analyses have revealed two paxillin-binding sites in the FAT domain of FAK. To define the role of paxillin binding to each site on FAK, point mutations have been engineered to specifically disrupt paxillin binding to each docking site on the FAT domain of FAK individually or in combination. RESULTS: These mutants have been characterized and reveal an important role for paxillin binding in FAK subcellular localization and signaling. One paxillin-binding site (comprised of alpha-helices 1 and 4 of the FAT domain) plays a more prominent role in localization than the other. Mutation of either paxillin-binding site has similar effects on FAK activation and downstream signaling. However, the sites aren't strictly redundant as each mutant exhibits phosphorylation/signaling defects distinct from wild type FAK and a mutant completely defective for paxillin binding. CONCLUSION: The studies demonstrate that the two paxillin-binding sites of FAK are not redundant and that both sites are required for FAK function.

A novel pathological role of p53 in kidney development revealed by gene-environment interactions.

Gene-environment interactions are implicated in congenital human disorders. Accordingly, there is a pressing need to develop animal models of human disease, which are the product of defined gene-environment interactions. Previously, our laboratory demonstrated that gestational salt stress of bradykinin B(2) receptor (B(2)R)-null mice induces renal dysgenesis and early death of the offspring. In contrast, salt-stressed B(2)R +/+ or +/- littermates have normal development. The present study investigates the mechanisms underlying the susceptibility of B(2)R-null mice to renal dysgenesis. Proteomic and conventional Western blot screens identified E-cadherin among the differentially repressed proteins in B(2)R-/- kidneys, whereas the checkpoint kinase Chk1 and its substrate P-Ser(20) p53 were induced. We tested the hypothesis that p53 mediates repression of E-cadherin gene expression and is causally linked to the renal dysgenesis. Genetic crosses between B(2)R -/- and p53+/- mice revealed that germline reduction of p53 gene dosage rescues B(2)R-/- mice from renal dysgenesis and restores kidney E-cadherin gene expression. Furthermore, gamma-irradiation induces repression of E-cadherin gene expression in p53+/+ but not -/- cells. In transient transfection assays, p53 repressed human E-cadherin promoter-driven reporter activity, whereas a mutant p53, which cannot bind DNA, did not. Functional promoter analysis indicated the presence of a p53-responsive element in exon 1, which partially mediates p53-induced repression. Chromatin immunoprecipitation assays revealed that p53 inhibits histone acetylation of the E-cadherin promoter. Treatment with a histone deacetylase inhibitor reversed both p53-mediated promoter repression and deacetylation. In conclusion, this study demonstrates that gene-environment interactions cooperate to induce congenital defects through p53 activation.