Biology subjects

Beane, W. S.

Publications and source records attributed to Beane, W. S..

3 recordsLinked to original sources

bioRxiv2025

Planar cell polarity signaling controls cell division symmetry to promote termination of adult tissue regeneration

Tissue formation is coordinated by cell-intrinsic and cell-extrinsic signals across space and time, yet how self-limiting growth is controlled remains mysterious. Here, we leveraged the highly regenerative planarian Schmidtea mediterranea to identify molecular regulators of endogenous growth termination in adults, where unchecked growth can promote carcinogenesis. We identified the Planar Cell Polarity (PCP) pathway as a key regulator of body-wide regenerative growth through control of stem cell division symmetry. Following PCP pathway inhibition, widespread tissue hyperplasia occurred weeks after regeneration normally finishes. Importantly, this was due to progenitor expansion and depletion of adult tspan-1+ pluripotent stem cells capable of whole-body regeneration. Using transcriptional analysis of regenerating animals over time, we identified that control of stem cell fate by changes in cell division symmetry is a potential growth termination mechanism. While symmetric divisions maintain the stem cell pool in adult planaria, upon PCP loss, the number of asymmetrically dividing cells increases, driving stem cell depletion and excessive tissue differentiation. Our data suggest that PCP signaling regulates stem cell maintenance and fate decisions during self-limiting growth. Summary StatementHere, we show that Planar Cell Polarity (PCP) signaling regulates stem cell division symmetry to control termination of adult tissue regeneration in planarians.

developmental biology↗

bioRxiv2024

Verification of radical pair mechanism predictions for weak magnetic field effects on superoxide in planarians

Superoxide concentration and tissue regeneration in planarians exhibit a complex non-monotonic dependence on the strength of an applied weak magnetic field. While this is difficult to understand based on classical physics, a recently proposed quantum model based on a flavinsuperoxide radical pair mechanism could replicate the previously observed superoxide concentrations. However, this model also predicts increased superoxide concentrations for both lower and higher fields. This seemed to conflict with earlier experimental observations on blastema sizes, which were correlated with superoxide in the previously observed regime but were known not to follow the predicted trends for lower and higher fields. Motivated by this apparent contradiction, we here directly experimentally tested the predictions of the quantum model for superoxide for lower and higher fields. To our own surprise, our experiments confirmed the predictions of the radical pair model for superoxide, and incorporating interactions with multiple nuclei further improved the models agreement with the experimental data. While open questions remain regarding the exact relationship between blastema sizes and superoxide, which is revealed to be more complex than previously observed, and the detailed properties of the underlying radical pair, our results significantly support a quantum biological explanation for the observed magnetic field effects.

biophysics↗

bioRxiv2022

Reactive Oxygen Species Signaling Differentially Controls Wound Healing and Regeneration

Reactive oxygen species (ROS), such as hydrogen peroxide, are conserved and critical components of both wound healing and regeneration. Even though millions are affected each year by poor wound healing and an inability to restore functional tissue, how the same ROS-mediated signaling regulates these two different processes is not fully understood. Here, we investigate the role(s) of ROS during planarian wound healing and regeneration. We show ROS accumulate after injury and are required for wound closure (by promoting cytoskeletal movements) and regrowth (by promoting blastema formation). We found that different threshold levels of ROS regulate separate downstream targets to control wound healing (jun-1) versus regeneration (hsp70). By only manipulating ROS levels, we were able to control which injury-induced program was initiated: failure to close (chronic wound), healing only (no blastema), or full regeneration. Our results demonstrate that healing versus regenerative outcomes are based on differential ROS-mediated gene expression soon after injury. This study highlights ROS signaling as a potential therapeutic means to control wound repair mechanisms in multiple contexts. Therefore, investigating the mechanisms by which ROS control different tissue repair processes will be necessary not only for regenerative medicine but to improve clinical outcomes for chronic wounds and fibrosis.

developmental biology↗