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Abstract With climate change impacting systems globally at alarming rates, the need for educating the next generation of environmental stewards is necessary. The Rocky Mountain Sustainability and Science Network (RMSSN) is an immersive field experience for undergraduate and graduate students interested in climate change and sustainability within National Parks. The program was established to educate and cultivate a diverse audience of future leaders, environmental guardians, and sustainability advocates with a focus on engaging underrepresented minorities (URM) in science. Participants were evaluated through efficacy instruments and focus groups to determine how a short‐term research experience could impact a student's future outlook and perceived ability to impact science and sustainability. Findings indicate URM, and majority students were more confident in their abilities, and more motivated to continue within their studies. RMSSN provides a framework that is translatable to other field‐based curriculums. This paper addresses specific engagement mechanisms for educating future science leaders. 

A comprehensive understanding of the mechanisms involved in epigenetic changes in gene expression is essential to the clinical management of diseases linked to the SMYD family of lysine methyltransferases. The five known SMYD enzymes catalyze the transfer of donor methyl groups from S-adenosylmethionine (SAM) to specific lysines on histones and non-histone substrates. SMYDs family members have distinct tissue distributions and tissue-specific functions, including regulation of development, cell differentiation, and embryogenesis. Diseases associated with SMYDs include the repressed transcription of SMYD1 genes needed for the formation of ion channels in the heart leading to heart failure, SMYD2 overexpression in esophageal squamous cell carcinoma (ESCC) or p53-related cancers, and poor prognosis associated with SMYD3 overexpression in more than 14 types of cancer including breast cancer, colon cancer, prostate cancer, lung cancer, and pancreatic cancer. Given the importance of epigenetics in various pathologies, the development of epigenetic inhibitors has attracted considerable attention from the pharmaceutical industry. The pharmacologic development of the inhibitors involves the identification of molecules regulating both functional SMYD SET (Suppressor of variegation, Enhancer of Zeste, Trithorax) and MYND (Myeloid-Nervy-DEAF1) domains, a process facilitated by available X-ray structures for SMYD1, SMYD2, and SMYD3. Important leads for potential pharmaceutical agents have been reported for SMYD2 and SMYD3 enzymes, and six epigenetic inhibitors have been developed for drugs used to treat myelodysplastic syndrome (Vidaza, Dacogen), cutaneous T-cell lymphoma (Zoinza, Isrodax), and peripheral T-cell lymphoma (Beleodag, Epidaza). The recently demonstrated reversal of SMYD histone methylation suggests that reversing the epigenetic effects of SMYDs in cancerous tissues may be a desirable target for pharmacological development. 

SMYD3 is a lysine methyltransferase that regulates the expression of over 80 genes and is required for the uncontrolled proliferation of most breast, colorectal, and hepatocellular carcinomas. The elimination of SMYD3 restores normal expression patterns of these genes and halts aberrant cell proliferation, making it a promising target for small molecule inhibition. In this study, we sought to establish a proof of concept for our in silico/in vitro hit-to-lead enzyme inhibitor development platform and to identify a lead small molecule candidate for SMYD3 inhibition. We used Schrodinger® software to screen libraries of small molecules in silico and the five compounds with the greatest predicted binding affinity within the SMYD3 binding pocket were purchased and assessed in vitro in direct binding assays and in breast cancer cell lines. We have confirmed the ability of one of these inhibitors, Inhibitor-4, to restore normal rates of cell proliferation, arrest the cell cycle, and induce apoptosis in breast cancer cells without affecting wildtype cell behavior. Our results provide a proof of concept for this fast and affordable small molecule hit-to-lead methodology as well as a promising candidate small molecule SMYD3 inhibitor for the treatment of human cancer. 

The Rocky Mountain Scholars Program (RMSP) was developed, in part, to improve student success and persistence in Engineering disciplines at Colorado State Universi-ty through a portfolio of engagement activities focused around undergraduate research experiences. Female RMSP participants exhibited substantially higher retention rates and grade point averages relative to other female engineering students at CSU. To better understand the impact of the RMSP, and its effectiveness among female engi-neering students, researchers focused on whether, and how, experiences and percep-tions differ between male and female students in engineering programs. That is, how do male and female students differ, if at all, in their subjective perception of life as an engineering major at CSU? A survey was developed measuring resilience, self-efficacy, motivation, social support, academic support, and perceived sexism. Data was obtained from 144 first-year engineering students at CSU. Results indicated that social support from extracurricular activities is particularly important among female students. This points to an increasing need for programs like the RMSP to create social networks among students and faculty, link students to the broader impacts of their work, and ultimately improve the undergraduate experience of under-represented groups in STEM programs. 

The SET and MYND domain-containing (SMYD) family of lysine methyltransferases are essential in several mammalian developmental pathways. Although predominantly expressed in the heart, the role of SMYD2 in heart development has yet to be fully elucidated and has even been shown to be dispensable in a murine Nkx2-5-associated conditional knockout. Additionally, SMYD2 was recently shown to be necessary not only for lymphocyte development but also for the viability of hematopoietic leukemias. Based on the broad expression pattern of SMYD2 in mammalian tissues, it is likely that it plays pivotal roles in a host of additional normal and pathological processes. In this brief review, we consider what is currently known about the normal and pathogenic functions of SMYD2 and propose specific future directions for characterizing its role in embryogenesis.