Am I a Science Person? A Strong Science Identity Bolsters Minority Students' Sense of Belonging and Performance in College.

Identifying as a "science person" is predictive of science success, but the mechanisms involved are not well-understood. We hypothesized that science identity predicts success because it fosters a sense of belonging in science classrooms. Thus, science identity should be particularly important for first-generation and racial-minority students, who may harbor doubts about belonging in science. Two field studies in college Introductory Biology classes (Ns = 368, 639) supported these hypotheses. A strong science identity predicted higher grades, particularly for minority students. Also consistent with hypotheses, Study 2 found that self-reported belonging in college mediated the relationship between science identity and performance. Furthermore, a social belonging manipulation eliminated the relationship between science identity and performance among minority students. These results support the idea that a strong science identity is particularly beneficial for minority students because it bolsters belonging in science courses. Practical and theoretical implications are discussed.

Changing Social Contexts to Foster Equity in College Science Courses: An Ecological-Belonging Intervention.

In diverse classrooms, stereotypes are often "in the air," which can interfere with learning and performance among stigmatized students. Two studies designed to foster equity in college science classrooms (Ns = 1,215 and 607) tested an intervention to establish social norms that make stereotypes irrelevant in the classroom. At the beginning of the term, classrooms assigned to an ecological-belonging intervention engaged in discussion with peers around the message that social and academic adversity is normative and that students generally overcome such adversity. Compared with business-as-usual controls, intervention students had higher attendance, course grades, and 1-year college persistence. The intervention was especially impactful among historically underperforming students, as it improved course grades for ethnic minorities in introductory biology and for women in introductory physics. Regardless of demographics, attendance in the intervention classroom predicted higher cumulative grade point averages 2 to 4 years later. The results illustrate the viability of an ecological approach to fostering equity and unlocking student potential.

New method for the orthogonal labeling and purification of Toxoplasma gondii proteins while inside the host cell.

UNLABELLED: Toxoplasma gondii is an obligate intracellular protozoan parasite that is capable of causing severe disease in immunocompromised humans. How T. gondii is able to modulate the host cell to support itself is still poorly understood. Knowledge pertaining to the host-parasite interaction could be bolstered by developing a system to specifically label parasite proteins while the parasite grows inside the host cell. For this purpose, we have created a strain of T. gondii that expresses a mutant Escherichia coli methionyl-tRNA synthetase (MetRS(NLL)) that allows methionine tRNA to be loaded with the azide-containing methionine analog azidonorleucine (Anl). Anl-containing proteins are susceptible to a copper-catalyzed "click" reaction to attach affinity tags for purification or fluorescent tags for visualization. The MetRS(NLL)-Anl system labels nascent T. gondii proteins in an orthogonal fashion, labeling proteins only in MetRS(NLL)-expressing parasites. This system should be useful for nonradioactive pulse-chase studies and purification of nascently translated proteins. Although this approach allows labeling of a diverse array of parasite proteins, secreted parasite proteins appear to be only minimally labeled in MetRS(NLL)-expressing T. gondii. The minimal labeling of secreted proteins is likely a consequence of the selective charging of the initiator tRNA (and not the elongator methionine tRNA) by the heterologously expressed bacterial MetRS. IMPORTANCE: Studying how T. gondii modifies the host cell to permit its survival is complicated by the complex protein environment of the host cell. The approach presented in this article provides the first method for specific labeling of T. gondii proteins while the parasite grows inside the host cell. We show that this approach is useful for pulse-chase labeling of parasite proteins during in vitro growth. It should also be applicable during in vivo infections and in other apicomplexan parasites, including Plasmodium spp.

Shroom3 functions downstream of planar cell polarity to regulate myosin II distribution and cellular organization during neural tube closure.

Neural tube closure is a critical developmental event that relies on actomyosin contractility to facilitate specific processes such as apical constriction, tissue bending, and directional cell rearrangements. These complicated processes require the coordinated activities of Rho-Kinase (Rock), to regulate cytoskeletal dynamics and actomyosin contractility, and the Planar Cell Polarity (PCP) pathway, to direct the polarized cellular behaviors that drive convergent extension (CE) movements. Here we investigate the role of Shroom3 as a direct linker between PCP and actomyosin contractility during mouse neural tube morphogenesis. In embryos, simultaneous depletion of Shroom3 and the PCP components Vangl2 or Wnt5a results in an increased liability to NTDs and CE failure. We further show that these pathways intersect at Dishevelled, as Shroom3 and Dishevelled 2 co-distribute and form a physical complex in cells. We observed that multiple components of the Shroom3 pathway are planar polarized along mediolateral cell junctions in the neural plate of E8.5 embryos in a Shroom3 and PCP-dependent manner. Finally, we demonstrate that Shroom3 mutant embryos exhibit defects in planar cell arrangement during neural tube closure, suggesting a role for Shroom3 activity in CE. These findings support a model in which the Shroom3 and PCP pathways interact to control CE and polarized bending of the neural plate and provide a clear illustration of the complex genetic basis of NTDs.