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The ability to strike a perceived sense of balance between work and life represents a challenge for many in academic and research sectors around the world. Before major shifts in the nature of academic work occurred, academia was historically seen as a rewarding and comparatively low-stress working environment [1]. Academics today need to manage many tasks during a workweek. The current academic working environment often prioritizes productivity over well-being, with researchers working long days, on weekends, on and off campus, and largely alone, potentially on tasks that may not be impactful. Academics report less time for research due to increasing administrative burden and teaching loads [1][2][3]. This is further strained by competition for job and funding opportunities [4,5], leading to many researchers spending significant time on applications, which takes away time from other duties such as performing research and mentorship [1,2]. The current hypercompetitive culture is particularly impactful on early career researchers (ECRs) employed on short-term contracts and is a major driver behind the unsustainable working hours reported in research labs around the world, increases in burnout, and decline in satisfaction with work-life balance [6][7][8][9][10]. ECRs may also find themselves constrained by the culture and management style of their laboratory and principal investigator (PI) [11][12]. Work-life balance can be defined as an individual's appraisal of how well they manage work-and nonwork-related obligations in ways that the individual is satisfied with both, while simultaneously maintaining their health and well-being [13]. Increasing hours at work can conflict with obligations outside of work, including but not limited to family care commitments, time with friends, time for self-care, and volunteering and community work. The increasing prevalence of technology that allows work to be out of the office can also exacerbate this conflict [14,15].The academic system's focus on publications and securing grant funding and academic positions instead of training, mentoring, and mental health has skewed the system negatively against prioritizing "The whole scientist" [5,16]. Research focused on the higher education sector has revealed that poor work-life balance can result in lower productivity and impact, stifled academic entrepreneurship, lower career satisfaction and success, lower organizational commitment, intention to leave academia, greater levels of burnout, fatigue and decreased social interactions, and poor physical and mental health, which has become increasingly prevalent among graduate students [1,[17][18][19][20][21][22]. For instance, a recent international survey of over 2,000 university staff views on work-life balance found that many academics feel stressed and underpaid and struggle to fit in time for personal relationships and family around their ever-growing

Tension of the actomyosin cell cortex plays a key role in determining cell–cell contact growth and size. The level of cortical tension outside of the cell–cell contact, when pulling at the contact edge, scales with the total size to which a cell–cell contact can grow [J.-L. Maître et al., Science 338, 253–256 (2012)]. Here, we show in zebrafish primary germ-layer progenitor cells that this monotonic relationship only applies to a narrow range of cortical tension increase and that above a critical threshold, contact size inversely scales with cortical tension. This switch from cortical tension increasing to decreasing progenitor cell–cell contact size is caused by cortical tension promoting E-cadherin anchoring to the actomyosin cytoskeleton, thereby increasing clustering and stability of E-cadherin at the contact. After tension-mediated E-cadherin stabilization at the contact exceeds a critical threshold level, the rate by which the contact expands in response to pulling forces from the cortex sharply drops, leading to smaller contacts at physiologically relevant timescales of contact formation. Thus, the activity of cortical tension in expanding cell–cell contact size is limited by tension-stabilizing E-cadherin–actin complexes at the contact.

Mentorship is experience and/or knowledge‐based guidance. Mentors support, sponsor and advocate for mentees. Having one or more mentors when you seek advice can significantly influence and improve your research endeavours, well‐being and career development. Positive mentee–mentor relationships are vital for maintaining work–life balance and success in careers. Early‐career researchers (ECRs), in particular, can benefit from mentorship to navigate challenges in academic and nonacademic life and careers. Yet, strategies for selecting mentors and maintaining interactions with them are often underdiscussed within research environments. In this Words of Advice, we provide recommendations for ECRs to seek and manage mentorship interactions. Our article draws from our experiences as ECRs and published work, to provide suggestions for mentees to proactively promote beneficial mentorship interactions. The recommended practices highlight the importance of identifying mentorship needs, planning and selecting multiple and diverse mentors, setting goals, and maintaining constructive, and mutually beneficial working relationships with mentors.

Metazoan development relies on the formation and remodeling of cell-cell contacts. Dynamic reorganization of adhesion receptors and the actomyosin cell cortex in space and time play a central role in cell-cell contact formation and maturation. Yet, how this process is mechanistically achieved remains unclear. Here, by building a biomimetic assay composed of progenitor cells adhering to supported lipid bilayers functionalized with E-cadherin ectodomains, we show that cortical Actin flows, driven by the depletion of Myosin-2 at the cell contact center, mediate the dynamic reorganization of adhesion receptors and cell cortex at the contact. E-cadherin-dependent downregulation of the small GTPase RhoA at the forming contact leads to both a depletion of Myosin-2 and a decrease of F-actin at the contact center. This depletion of Myosin-2 causes centrifugal F-actin flows, leading to further accumulation of F-actin at the contact rim and the progressive redistribution of E-cadherin from the contact center to the rim. Eventually, this combination of actomyosin downregulation and flows at the contact determine the characteristic molecular organization, with E-cadherin and F-actin accumulating at the contact rim, where they are needed to mechanically link the contractile cortices of the adhering cells.