Flexible and Family-Friendly Policies at Utah’s “Best Places to Work”

The COVID-19 pandemic that reached Utah in March of 2020 has had an enormous impact on the way companies do business. Perhaps the biggest change for employees came in the widespread shift to remote work as a public health measure, but many companies adjusted work practices and policies in other ways to support their employees during a challenging time. Many changes focus on flexibility and family-friendly policies, which have traditionally been a double-edged sword for working women. Though such offerings have made it possible for some mothers to remain in the workforce, taking advantage of such programs has often placed women on the “mommy-track,” where they are seen as being less committed to their careers. Yet these programs are not for women only, and men who utilize family-friendly benefits have also experienced backlash

Flexible and Family-Friendly Policies at Utah\u27s Best Places to Work

The COVID-19 pandemic that reached Utah in March of 2020 has had an enormous impact on the way companies do business. Perhaps the biggest change for employees came in the widespread shift to remote work as a public health measure, but many companies adjusted work practices and policies in other ways to support their employees during a challenging time. Many changes focus on flexibility and family-friendly policies, which have traditionally been a double-edged sword for working women. Though such offerings have made it possible for some mothers to remain in the workforce, taking advantage of such programs has often placed women on the mommy-track, where they are seen as being less committed to their careers. Yet these programs are not for women only, and men who utilize family-friendly benefits have also experienced backlash

Coordination by Cdc42 of actin, contractility, and adhesion for melanoblast movement in mouse skin

YesThe individual molecular pathways downstream of Cdc42, Rac, and Rho GTPases are well documented, but we know surprisingly little about how these pathways are coordinated when cells move in a complex environment in vivo. In the developing embryo, melanoblasts originating from the neural crest must traverse the dermis to reach the epidermis of the skin and hair follicles. We previously established that Rac1 signals via Scar/WAVE and Arp2/3 to effect pseudopod extension and migration of melanoblasts in skin. Here we show that RhoA is redundant in the melanocyte lineage but that Cdc42 coordinates multiple motility systems independent of Rac1. Similar to Rac1 knockouts, Cdc42 null mice displayed a severe loss of pigmentation, and melanoblasts showed cell-cycle progression, migration, and cytokinesis defects. However, unlike Rac1 knockouts, Cdc42 null melanoblasts were elongated and displayed large, bulky pseudopods with dynamic actin bursts. Despite assuming an elongated shape usually associated with fast mesenchymal motility, Cdc42 knockout melanoblasts migrated slowly and inefficiently in the epidermis, with nearly static pseudopods. Although much of the basic actin machinery was intact, Cdc42 null cells lacked the ability to polarize their Golgi and coordinate motility systems for efficient movement. Loss of Cdc42 de-coupled three main systems: actin assembly via the formin FMNL2 and Arp2/3, active myosin-II localization, and integrin-based adhesion dynamics.Cancer Research UK (to L.M.M. [A17196], R.H.I. [A19257], and S.W.G.T.) and NIH grants P01-GM103723 and P41-EB002025 (to K.M.H.). N.R.P. is supported by a Pancreatic Cancer Research Fund grant (to L.M.M.). Funding to Prof. Rottner by the Deutsche Forschungsgemeinschaft (grant RO2414/3-2)

Parallel Evolution of Tobramycin Resistance Across Species and Environments

Different species exposed to a common stress may adapt by mutations in shared pathways or in unique systems, depending on how past environments have molded their genomes. Understanding how diverse bacterial pathogens evolve in response to an antimicrobial treatment is a pressing example of this problem, where discovery of molecular parallelism could lead to clinically useful predictions. Evolution experiments with pathogens in environments containing antibiotics, combined with periodic whole-population genome sequencing, can be used to identify many contending routes to antimicrobial resistance. We separately propagated two clinically relevant Gram-negative pathogens, Pseudomonas aeruginosa and Acinetobacter baumannii, in increasing concentrations of tobramycin in two different environments each: planktonic and biofilm. Independently of the pathogen, the populations adapted to tobramycin selection by parallel evolution of mutations in fusA1, encoding elongation factor G, and ptsP, encoding phosphoenolpyruvate phosphotransferase. As neither gene is a direct target of this aminoglycoside, mutations to either are unexpected and underreported causes of resistance. Additionally, both species acquired antibiotic resistance-associated mutations that were more prevalent in the biofilm lifestyle than in the planktonic lifestyle; these mutations were in electron transport chain components in A. baumannii and lipopolysaccharide biosynthesis enzymes in P. aeruginosa populations. Using existing databases, we discovered site-specific parallelism of fusA1 mutations that extends across bacterial phyla and clinical isolates. This study suggests that strong selective pressures, such as antibiotic treatment, may result in high levels of predictability in molecular targets of evolution, despite differences between organisms’ genetic backgrounds and environments

Dedication

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