Although bioinformatics is becoming increasingly central to research in the life sciences, bioinformatics skills and knowledge are not well integrated into undergraduate biology education. This curricular gap prevents biology students from harnessing the full potential of their education, limiting their career opportunities and slowing research innovation. To advance the integration of bioinformatics into life sciences education, a framework of core bioinformatics competencies is needed. To that end, we here report the results of a survey of biology faculty in the United States about teaching bioinformatics to undergraduate life scientists. Responses were received from 1,260 faculty representing institutions in all fifty states with a combined capacity to educate hundreds of thousands of students every year. Results indicate strong, widespread agreement that bioinformatics knowledge and skills are critical for undergraduate life scientists as well as considerable agreement about which skills are necessary. Perceptions of the importance of some skills varied with the respondent’s degree of training, time since degree earned, and/or the Carnegie Classification of the respondent’s institution. To assess which skills are currently being taught, we analyzed syllabi of courses with bioinformatics content submitted by survey respondents. Finally, we used the survey results, the analysis of the syllabi, and our collective research and teaching expertise to develop a set of bioinformatics core competencies for undergraduate biology students. These core competencies are intended to serve as a guide for institutions as they work to integrate bioinformatics into their life sciences curricula.

Bioinformatics, a discipline that combines aspects of biology, statistics, mathematics, and computer science, is becoming increasingly important for biological research. However, bioinformatics instruction is not yet generally integrated into undergraduate life sciences curricula. To understand why we studied how bioinformatics is being included in biology education in the US by conducting a nationwide survey of faculty at two- and four-year institutions. The survey asked several open-ended questions that probed barriers to integration, the answers to which were analyzed using a mixed-methods approach. The barrier most frequently reported by the 1,260 respondents was lack of faculty expertise/training, but other deterrents—lack of student interest, overly-full curricula, and lack of student preparation—were also common. Interestingly, the barriers faculty face depended strongly on whether they are members of an underrepresented group and on the Carnegie Classification of their home institution. We were surprised to discover that the cohort of faculty who were awarded their terminal degree most recently reported the most preparation in bioinformatics but teach it at the lowest rate.

To examine the functions of the Arf‐like protein, Arl1p, in Saccharomyces cerevisiae, a null allele, arl1Δ::HIS3, was constructed in two strains. In one background only, loss of ARL1 resulted in temperature‐sensitive (ts) growth (suppressed on high‐osmolarity media). Allelic variation at the SSD1 locus accounted for differences between strains. Strains lacking ARL1 exhibited several defects in membrane traffic. First, arl1Δ strains secreted less protein as measured by TCA‐precipitable radioactivity found in the media of [³⁵S]‐labelled cells. A portion of newly synthesized carboxypeptidase Y (CPY) was secreted rather than correctly targeted to the vacuole. Uptake of the fluid‐phase marker, lucifer yellow, was reduced. All these phenotypes were exacerbated in an ssd1 background. The ts phenotype of the arl1Δssd1 strain was suppressed by YPT1, the yeast Rab1a homologue, suggesting that ARL1 and YPT1 have partially overlapping functions. These findings demonstrate that ARL1 encodes a regulator of membrane traffic. Copyright © 2002 John Wiley & Sons, Ltd.

The preparation of future scientists, the technical workforce, and informed citizens will require continued transformation to the ways we approach STEM teaching and learning. Undergraduate STEM education is rapidly emerging as a focus of faculty scholarship, but new models for reform need to be developed and tested to accelerate changes in teaching practices. This paper describes a flexible, participant-driven, multi-phase, collaborative approach to developing open educational resources (OERs) that leverages linked communities of practice (CoPs). Equally valuable, our framework for development, adaptation, dissemination, and validation of OERs provides a platform for faculty professional development and sustained support through cooperative mentoring. The three linked CoPs in the framework include incubators for the creation of initial OERs, Faculty Mentoring Networks (FMNs) for the implementation and adaptation of OERs for classroom use, and Education Research Communities to assess the effectiveness of the OERs. The CoPs create numerous benefits for participating faculty, including the ability to collaborate in the Scholarship of Teaching and Learning (SoTL) through scholarly publication of OERs and their assessment; ongoing mentorship in implementation of OERs in the classroom; and development of educational leadership skills and experience. Thus, the three CoPs synergize with one another to build and sustain capacity through providing vetted, up-to-date educational resources, as well as ongoing training and support for faculty. While we developed this approach for the rapidly changing field of bioinformatics, the linked CoP framework will have utility for STEM education reform more broadly and disciplines beyond STEM.

Macroautophagy/autophagy is a cellular degradation process that sequesters organelles or proteins into a double-membrane structure called the phagophore; this transient compartment matures into an autophagosome, which then fuses with the lysosome or vacuole to allow hydrolysis of the cargo. Factors that control membrane traffic are also essential for each step of autophagy. Here we demonstrate that 2 monomeric GTP-binding proteins in Saccharomyces cerevisiae, Arl1 and Ypt6, which belong to the Arf/Arl/Sar protein family and the Rab family, respectively, and control endosome-trans-Golgi traffic, are also necessary for starvation-induced autophagy under high temperature stress. Using established autophagy-specific assays we found that cells lacking either ARL1 or YPT6, which exhibit synthetic lethality with one another, were unable to undergo autophagy at an elevated temperature, although autophagy proceeds normally at normal growth temperature; specifically, strains lacking one or the other of these genes are unable to construct the autophagosome because these 2 proteins are required for proper traffic of Atg9 to the phagophore assembly site (PAS) at the restrictive temperature. Using degron technology to construct an inducible arl1Δ ypt6Δ double mutant, we demonstrated that cells lacking both genes show defects in starvation-inducted autophagy at the permissive temperature. We also found Arl1 and Ypt6 participate in autophagy by targeting the Golgi-associated retrograde protein (GARP) complex to the PAS to regulate the anterograde trafficking of Atg9. Our data show that these 2 membrane traffic regulators have novel roles in autophagy.