Biology subjects

Eaton, C. D.

Publications and source records attributed to Eaton, C. D..

3 recordsLinked to original sources

bioRxiv2023

Detecting signals of critical transition in inclusive teaching in biology education: A computational text analysis of CourseSource

We examine every Inclusive Teaching section in articles published by the journal CourseSource - undergraduate biology teaching materials and related essays - from 2014 to 2022 to understand the evolution of inclusive teaching ideas as expressed through language. We find a rapid shift in attention to inclusive teaching occurs between 2018 and 2019, marked by an increase in section length, increased use of inclusive teaching keywords, and an increase in complexity of ideas in the semantic network. This critical transition occurs before many of the recent events in 2020 which have renewed conversation on equity in education. Some effect is associated with Writing Workshop Faculty Mentoring Networks, which provide participants with authoring resources and support. However, this alone is not enough to explain the observed shift, suggesting that many other structures, conversations, and investments were already providing the fertile ground for educational equity in biology education.

scientific communication and education↗

bioRxiv2023

A protein hydroxylase couples epithelial membrane biology to nucleolar ribosome biogenesis

Jumonji-C (JmjC) ribosomal protein hydroxylases are an ancient class of oxygen- and Fe(II)-dependent oxygenases that spawned the wider JmjC family and Histone Lysine Demethylases (KDMs) in eukaryotes. Myc-induced Antigen (MINA) has been implicated in ribosome biogenesis and was assigned as a nucleolar-localized JmjC histidyl hydroxylase of the large ribosomal subunit protein RPL27A, consistent with reports that it supports cell growth and viability in a variety of tumor cell types. Reported roles in diverse aspects of disease biology may be consistent with additional MINA functions, although the molecular mechanisms involved remain unclear. Here, we describe an extra-nucleolar interaction of MINA with the Hinge domain of the membrane-associated guanylate kinase, MPP6. We show that MINA promotes the expression and membrane localization of MPP6 and that the MINA-MPP6 pathway is required for epithelial tight junction integrity and barrier function. The function of MINA in this novel pathway is suppressed by ribosomal RNA transcription and the nucleolar MINA interactome. In this way, MINA couples epithelial membrane biology to nucleolar ribosome biogenesis. Our work sheds light on how quiescent cells lose adhesion as they switch to proliferative states associated with increased ribosome biogenesis.

cell biology↗

bioRxiv2022

Epigenetic reprogramming shapes the cellular landscape of schwannoma

Cell state evolution underlies tumor development and response to therapy1, but mechanisms specifying cancer cell states and intratumor heterogeneity are incompletely understood. Schwannomas are the most common tumors of the peripheral nervous system and are treated with surgery and ionizing radiation2-5. Schwannomas can oscillate in size for many years after radiotherapy6,7, suggesting treatment may reprogram schwannoma cells or the tumor microenvironment. Here we show epigenetic reprogramming shapes the cellular landscape of schwannomas. We find schwannomas are comprised of 2 molecular groups distinguished by reactivation of neural crest development pathways or misactivation of nerve injury mechanisms that specify cancer cell states and the architecture of the tumor immune microenvironment. Schwannoma molecular groups can arise independently, but ionizing radiation is sufficient for epigenetic reprogramming of neural crest to immune-enriched schwannoma by remodeling chromatin accessibility, gene expression, and metabolism to drive schwannoma cell state evolution and immune cell infiltration. To define functional genomic mechanisms underlying epigenetic reprograming of schwannomas, we develop a technique for simultaneous interrogation of chromatin accessibility and gene expression coupled with genetic and therapeutic perturbations in single-nuclei. Our results elucidate a framework for understanding epigenetic drivers of cancer evolution and establish a paradigm of epigenetic reprograming of cancer in response to radiotherapy.

cancer biology↗