Ras1 is a small GTPase in the budding yeast Saccharomyces cerevisiae that regulates nutrient signaling. It has been shown that Ras1 undergoes phosphorylation, but the functional consequences and regulation of Ras1 phosphorylation remain unknown. Here we identify Ser-226 as an important residue for Ras1 phosphorylation, as mutating this residue to an alanine drastically diminishes the level of Ras1 phosphorylation. Notably, phosphorylated Ras1 accumulates as the cells approach the stationary phase of growth. Likewise, subjecting cells to nitrogen starvation also elevates the level of Ras1 phosphorylation. Interestingly, blocking Ras1 phosphorylation diminishes the level of autophagy and also renders the cells more sensitive to heat shock. Together, these data suggest a role of Ras1 phosphorylation in modulating nutrient signaling and stress response.
Iron progressively accumulates with age and can be further exacerbated by dietary iron intake, genetic factors, and repeated blood transfusions. While iron plays a vital role in various physiological processes within the human body, its accumulation contributes to cellular aging in several species. In its free form, iron can initiate the formation of free radicals at a cellular level and contribute to systemic disorders. This is most evident in high iron conditions such as hereditary hemochromatosis, when accumulation of iron contributes to the development of arthritis, cirrhosis, or cardiomyopathy. A growing body of research has further identified iron’s contributory effects in neurodegenerative diseases, ocular disorders, cancer, diabetes, endocrine dysfunction, and cardiovascular diseases. Reducing iron levels by repeated phlebotomy, iron chelation, and dietary restriction are the common therapeutic considerations to prevent iron toxicity. Chelators such as deferoxamine, deferiprone, and deferasirox have become the standard of care in managing iron overload conditions with other potential applications in cancer and cardiotoxicity. In certain animal models, drugs with iron chelating ability have been found to promote health and even extend lifespan. As we further explore the role of iron in the aging process, iron chelators will likely play an increasingly important role in our health.
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Objective This article assesses recent trends in tenure length for chairs of academic departments of ophthalmology. Materials and Methods This is a cross-sectional study of current chairs from 136 institutions. Questionnaires emailed to ophthalmology chairs assessed duration of tenure and demographics of current and previous chairs. Based off of this data, trends in tenure length, turnover rates, and retention rates were determined. Results From 1998 to 2018, 255 individuals held the position of chair at 95 academic departments of ophthalmology. Mean tenure length was 17.8 years for chairs whose tenure included 2005, and decreased to 15.2 and 10.4 years for chairs whose tenures included 2010 and 2015, respectively. Mean annual turnover began at 5.3% in the first 5 years of the study, increasing to 6.5% in the following 5 years before returning to a baseline of 5.3% in the past 5 years. An average turnover of 5.2% was demonstrated during the entire study period. Five-year retention rates for new chairs averaged at 86.2%. Representation of female chairs rose from values of 2.1 and 3.1% in the beginning of the period to 7.3 and 8.4% in 2015 and 2016, respectively. Conclusions The average turnover rate for chairs of ophthalmology has remained stable over the past 20 years, with an observed slight decrease in mean tenure length. This stability is welcomed in the wake of predicted turnover within the field of ophthalmology, but continued assessment and preventative policies should be maintained to continue current trends.
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