RESUMO
Problem: Medical students experience racial and sociopolitical trauma that disrupts their learning and wellbeing. Intervention: University of California, San Francisco (UCSF) School of Medicine students advocated for a systems approach to responding to traumatic events. Students partnered with educators to introduce an innovative protocol that affords short-term flexibility in curricular expectations (e.g., defer attendance, assignments, assessments) to empower students to rest, gather, or pursue community advocacy work. This study explored students' protocol utilization and student, staff, and faculty experience with its implementation. Context: UCSF is a public medical school with a diverse student body. Students raised the need to acknowledge the effects of trauma on their learning and wellbeing. Consequently, students and educators created the UCSF Racial and Sociopolitical Trauma protocol ('protocol') to allow students time-limited flexibility around academic obligations following events anticipated to inflict trauma on a school community level. The protocol affords students space to process events and engage with affected communities while ensuring all students achieve school competencies and graduation requirements. Impact: We conducted a two-phase mixed methods study: (1) retrospective analysis of quantitative data on students' protocol use and (2) focus groups with students, staff, and faculty. We used descriptive statistics to summarize students' protocol use to adjust attendance, assignment submission, and assessments and thematic analysis of focus group data. Across eight protocol activations June 2020 - November 2021, 357 of 664 (54%) students used it for 501 curricular activities: 56% (n = 198) for attendance, 71% (n = 252) for assignments, and 14% (n = 51) for assessments. When deciding to utilize the protocol, student focus group participants considered sources of restoration; impact on their curricular/patient responsibilities; and their identities. The protocol symbolized an institutional value system that made students feel affirmed and staff and faculty proud. Staff and faculty initially faced implementation challenges with questions around how to apply the protocol to curricular components and how it would affect their roles; however, these questions became clearer with each protocol activation. Questions remain regarding how the protocol can be best adapted for the clerkship setting. Lessons Learned: High protocol usage and focus group data confirmed that students found value in the protocol, and staff and faculty felt invested in the protocol mission. This student-initiated intervention supports a cultural shift beyond diversity toward trauma-informed medical education. Partnership among learners and educators can contribute to transforming learning and healthcare environments by enacting systems and structures that enable all learners to thrive.
RESUMO
Evolutionarily conserved polo-like kinase, Cdc5 (Plk1 in humans), associates with kinetochores during mitosis; however, the role of cell cycle-dependent centromeric ( CEN) association of Cdc5 and its substrates that exclusively localize to the kinetochore have not been characterized. Here we report that evolutionarily conserved CEN histone H3 variant, Cse4 (CENP-A in humans), is a substrate of Cdc5, and that the cell cycle-regulated association of Cse4 with Cdc5 is required for cell growth. Cdc5 contributes to Cse4 phosphorylation in vivo and interacts with Cse4 in mitotic cells. Mass spectrometry analysis of in vitro kinase assays showed that Cdc5 phosphorylates nine serine residues clustered within the N-terminus of Cse4. Strains with cse4-9SA exhibit increased errors in chromosome segregation, reduced levels of CEN-associated Mif2 and Mcd1/Scc1 when combined with a deletion of MCM21. Moreover, the loss of Cdc5 from the CEN chromatin contributes to defects in kinetochore integrity and reduction in CEN-associated Cse4. The cell cycle-regulated association of Cdc5 with Cse4 is essential for cell viability as constitutive association of Cdc5 with Cse4 at the kinetochore leads to growth defects. In summary, our results have defined a role for Cdc5-mediated Cse4 phosphorylation in faithful chromosome segregation.