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Hernandez, P. R.

Publications and source records attributed to Hernandez, P. R..

3 recordsLinked to original sources

What drives change? Characterizing scientific self-efficacy development in undergraduate research experiences

Undergraduate research experiences (UREs) and course-based UREs (CUREs) promote students scientific self-efficacy growth. Yet, how self-efficacy develops during research is not understood. Furthermore, what students do during research varies in ways that likely affect self-efficacy development. We sought to address these knowledge gaps by collecting scientific self-efficacy data from CURE and URE students at nine universities at the beginning, middle, and end of a single term of research. We leveraged a theoretical advancement, latent state-trait theory-revised, to disaggregate the components of students self-efficacy into stable or trait-like self-efficacy and dynamic or state-like self-efficacy. We determined that students scientific self-efficacy was moderately stable during their research, with the most malleable component being beliefs in their abilities to figure out data collection and explain results. We also surveyed students [~]45 times throughout their research experience to test the extent to which research hours and types of research tasks contributed to self-efficacy development. We found that students who completed more analytic tasks experienced significantly more self-efficacy growth than students who completed other types of tasks, while time spent on research was not influential. Our results illustrate the importance of engaging students in analytic tasks during CUREs and UREs for fostering their self-efficacy development. Highlight for table of contentsUsing latent state-trait theory-revised, we found that students scientific self-efficacy was more stable than malleable over one research term. Beliefs about data collection and explaining results were most dynamic. Conducting more analytic tasks fostered self-efficacy, while the time spent and completion of other tasks had no effect.

scientific communication and education↗

Rapidly evolving orphan immunity genes protect human gut bacteria from intoxication by the type VI secretion system

Bacteria encode diverse mechanisms for mediating interbacterial antagonism through the exchange of toxic effector proteins. Although the structure, function, and regulation of these pathways has been well established for many organisms, an understanding of their ecological and evolutionary dynamics lags behind. Type VI secretion systems (T6SS) deliver effectors between competing Gram-negative bacteria, including among mammalian gut Bacteroidales, resulting in the evolution of elaborate defense mechanisms that protect against T6SS attack. One such mechanism is the recombinase-associated acquired interbacterial defence (rAID) system, which harbors arrays of orphan immunity genes that diverge in sequence from T6SS-associated cognate immunity genes. It is not known if such sequence divergence impacts rAID orphan immunity function, or how rAID distribution across microbiomes relates to the T6SS. Here, we show that divergent rAID orphan immunity factors that possess SUKH domains allow bacteria to survive intoxication by cognate effectors. Such protection is due to high affinity protein-protein interactions between orphan immunity and effector that are comparable to that of cognate effector-immunity. Unlike other examples of T6SS effector-immunity interactions, we find that the binding interface is comprised of electrostatic interactions with a high degree of redundancy underlying its protective capacity. Finally, we quantify orphan immunity and effector gene abundance and dynamics across human gut metagenomes, revealing patterns of co-occurrence indicative of positive selection. Population genetic analyses of longitudinal data suggests that orphan immunity genes accumulate non-synonymous mutations that lie at the predicted effector-immunity interface. Together, our findings establish rAID orphan immunity genes as important bacterial fitness determinants in the human gut.

microbiology↗

Tiny Earth CURE improves student persistence in science

Course-based undergraduate research experiences (CUREs) enhance student retention in STEM, particularly among students who belong to historically excluded communities. Yet the mechanisms by which CUREs contribute to student integration and persistence are poorly understood. Utilizing the Tripartite Integration Model of Social Influence (TIMSI), this longitudinal study examines how Tiny Earth, an antibiotic-discovery CURE, impacts students scientific self-efficacy, scientific identity, endorsement of scientific community values, and intentions to persist in science. The study also explores how gains in TIMSI factors vary as a function of student demographics and course characteristics. Results of pre-and post-course measurements show that scientific self-efficacy and identity increased among students in Tiny Earth, and some student demographics and course characteristics moderated these gains. Gains in scientific self-efficacy, identity, and values correlated with gains in persistence intentions, whereas student demographics and course characteristics did not. Results of this study show that the Tiny Earth CURE enhanced students integration into the scientific community, which was linked to intentions of students of both historically underrepresented and majority groups to persist in STEM. We discuss how courses that provide opportunity to learn science skills in the context of a CURE can contribute toward enlarging and diversifying the STEM workforce.

scientific communication and education↗