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Undergraduate research experience has been shown to enhance student learning and improve persistence in science, technology, engineering, and mathematics (STEM). Researchers studying undergraduate research experiences have largely focused on student outcomes and have seldom investigated the outcomes of graduate and postdoctoral mentors. Here, we report a non-credit, year-long mentor professional development program designed for graduate students, postdoctoral scholars, and research staff in STEM. Mentors attended a series of six interactive and discussion-based workshops and mentored first-year undergraduate students in independent summer research projects. We report evaluation findings for three mentor cohorts using a combination of qualitative analysis of mentoring philosophies and quantitative assessment of pre- and post-surveys about mentoring objectives and skills. Results indicate that mentors gained self-efficacy in some objectives and skills. However, many other objectives and skills remained unchanged. We explore possible explanations for the lack of more broad-scale gains across survey items and present ideas for program improvement.

Undergraduate research experiences may increase persistence in STEM majors. We describe a research program that targets first-year students selected for their curiosity and attitudes towards science. We explain the implementation of the program over 3 years and present evaluation data using a group of matched controls. Participants and controls pursued STEM degrees at equivalent rates, but participants were significantly more involved in research. Initial laboratory interest and mentor pairing may have played a role in this finding. Female participants, particularly those with male laboratory mentors, engaged in more research than men.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2010.05.504 Byline: Bernadette M. Glasheen (a), Renee M. Robbins (b), Caitlin Piette (a), Greg J. Beitel (b), Andrea Page-McCaw (a) Keywords: Tracheae; Remodeling; Extracellular matrix; Tube elongation; Matrix metalloproteinases (MMPs); Drosophila; Cuticle; Molting; Fusion cell Abstract: Organ size typically increases dramatically during juvenile growth. This growth presents a fundamental tension, as organs need resiliency to resist stresses while still maintaining plasticity to accommodate growth. The extracellular matrix (ECM) is central to providing resiliency, but how ECM is remodeled to accommodate growth is poorly understood. We investigated remodeling of Drosophila respiratory tubes (tracheae) that elongate continually during larval growth, despite being lined with a rigid cuticular ECM. Cuticle is initially deposited with a characteristic pattern of repeating ridges and valleys known as taenidia. We find that for tubes to elongate, the extracellular protease Mmp1 is required for expansion of ECM between the taenidial ridges during each intermolt period. Mmp1 protein localizes in periodically spaced puncta that are in register with the taenidial spacing. Mmp1 also degrades old cuticle at molts, promotes apical membrane expansion in larval tracheae, and promotes tube elongation in embryonic tracheae. Whereas work in other developmental systems has demonstrated that MMPs are required for axial elongation occurring in localized growth zones, this study demonstrates that MMPs can also mediate interstitial matrix remodeling during growth of an organ system. Author Affiliation: (a) Department of Biology and Center for Biotechnology and Interdisciplinary Studies, Rensselaer Polytechnic Institute, Troy, NY 12180, USA (b) Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, IL 60208, USA Article History: Received 30 October 2009; Revised 10 May 2010; Accepted 24 May 2010

The integrity of polarized epithelia is critical for development and human health. Many questions remain concerning the full complement and the function of the proteins that regulate cell polarity (1). Here we report that the Drosophila FERM proteins Yurt (Yrt) (2) and Coracle (Cora) (3) and the membrane proteins Neurexin IV (Nrx-IV) (4) and [Na.sup.+],[K.sup.+]-ATPase (5) are a new group of functionally cooperating epithelial polarity proteins. This 'Yrt/Cora group' promotes basolateral membrane stability and shows negative regulatory interactions with the apical determinant Crumbs (Crb). Genetic analyses indicate that Nrx-IV and [Na.sup.+],[K.sup.+]-ATPase act together with Cora in one pathway, whereas Yrt acts in a second redundant pathway. Moreover, we show that the Yrt/Cora group is essential for epithelial polarity during organogenesis but not when epithelial polarity is first established or during terminal differentiation. This property of Yrt/Cora group proteins explains the recovery of polarity in embryos lacking the function of the Lethal giant larvae (Lgl) group of basolateral polarity proteins (6,7). We also find that the mammalian Yrt orthologue EPB41L5 (also known as YMO1 and Limulus) (8-10) is required for lateral membrane formation, indicating a conserved function of Yrt proteins in epithelial polarity., To clarify the mechanisms of epithelial polarization, we analysed the function of the FERM-domain protein Yrt, which was shown to act as a negative regulatory component of the Crb complex [...]

The molecular mechanisms that enable multicellular organisms to sense and modulate their responses to hyperosmotic environments are poorly understood. Here, we employ Caenorhabditis elegans to characterize the response of a multicellular organism to osmotic stress and establish a genetic screen to isolate mutants that are osmotic stress resistant (OSR). In this study, we describe the cloning of a novel gene, osr-1, and demonstrate that it regulates osmosensation, adaptation, and survival in hyperosmotic environments. Whereas wild-type animals exposed to hyperosmotic conditions rapidly lose body volume, motility, and viability, osr-1(rm1) mutant animals maintain normal body volume, motility, and viability even upon chronic exposures to high osmolarity environments. In addition, os-1(rm1) animals are specifically resistant to osmotic stress and are distinct from previously characterized osmotic avoidance defective (OSM) and general stress resistance age-1(hx546) mutants. OSR-1 is expressed in the hypodermis and intestine, and expression of OSR-1 in hypodermal cells rescues the osr-1(rm1) phenotypes. Genetic epistasis analysis indicates that OSR-1 regulates survival under osmotic stress via CaMKII and a conserved p38 MAP kinase signaling cascade and regulates osmotic avoidance and resistance to acute dehydration likely by distinct mechanisms. We suggest that OSR-1 plays a central role in integrating stress detection and adaptation responses by invoking multiple signaling pathways to promote survival under hyperosmotic environments.

Genetic analysis of lin-1 loss-of-function mutations suggests that lin-1 controls multiple cell-fate decisions during Caenorhabditis elegans development and is negatively regulated by a conserved receptor tyrosine kinase-Ras-ERK mitogen-activated protein (MAP) kinase signal transduction pathway. LIN-1 protein contains an ETS domain and presumably regulates transcription. We identified and characterized six gain-of-function mutations that define a new class of lin-1 allele. These lin-1 alleles appeared to be constitutively active and unresponsive to negative regulation. Each allele has a single-base change that affects the predicted C terminus of LIN-1, suggesting this region is required for negative regulation. The C terminus of LIN-1 was a high-affinity substrate for Erk52 in vitro, suggesting that LIN-1 is directly regulated by ERK MAP kinase. Because mpk-1 ERK MAP kinase controls at least one cell-fate decision that does not require lin-1, our results suggest that MPK-1 contributes to the specificity of this receptor tyrosine kinase-Ras-MAP kinase signal transduction pathway by phosphorylating different proteins in different developmental contexts. These lin-1 mutations all affect a four-amino-acid motif, FQFP, that is conserved in vertebrate and Drosophila ETS proteins that are also phosphorylated by ERK MAP kinase. This sequence may be a substrate recognition motif for the ERK subfamily of MAP kinases.

We report new [w.sup.-] fluorescent balancers scorable from stage 13 through adulthood that bear a nuclearlocalized yellow fluorescent protein marker directly driven by dfd and GMR enhancer elements. The utility of this marker is enhanced by identification of an anti-GFP/yellow fluorescent protein (YFP) serum that is compatible with heat fixation.

Biological tubes are essential for animal survival, and their functions are dependent on tube shape. Analyzing the contributions of cell shape and organization to the morphogenesis of small tubes has been hampered by the limitations of existing programs in quantifying cell geometry on highly curved tubular surfaces and calculating tubespecific parameters. We therefore developed QuBiT (Quantitative Tool for Biological Tubes) and used it to analyze morphogenesis of the embryonic Drosophila trachea (airway). In the main tube, we find previously unknown anterior-to-posterior (A-P) gradients of cell apical orientation and aspect ratio, and periodicity in the organization of apical cell surfaces. Inferred cell intercalation during development dampens an A-P gradient of the number of cells per cross-section of the tube, but does not change the patterns of cell connectivity. Computationally 'unrolling' the apical surface of wild-type trachea and the hindgut reveals previously unrecognized spatial patterns of the apical marker Uninflatable and a non-redundant role for the Na+/K+ ATPase in apical marker organization. These unexpected findings demonstrate the importance of a computational tool for analyzing small diameter biological tubes. [ABSTRACT FROM AUTHOR]

Patients with severe lung disease may develop hypercapnia, elevation of the levels of CO2 in the lungs and blood, which is associated with increased risk of death, often from infection. To identify compounds that ameliorate the adverse effects of hypercapnia, we performed a focused screen of 8832 compounds using a CO2-responsive luciferase reporter in Drosophila S2* cells. We found that evoxine, a plant alkaloid, counteracts the CO2-induced transcriptional suppression of antimicrobial peptides in S2* cells. Strikingly, evoxine also inhibits hypercapnic suppression of interleukin-6 and the chemokine CCL2 expression in human THP-1 macrophages. Evoxine’s effects are selective, since it does not prevent hypercapnic inhibition of phagocytosis by THP-1 cells or CO2-induced activation of AMPK in rat ATII pulmonary epithelial cells. The results suggest that hypercapnia suppresses innate immune gene expression by definable pathways that are evolutionarily conserved and demonstrate for the first time that specific CO2 effects can be targeted pharmacologically. [ABSTRACT FROM AUTHOR]