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The COVID-19 pandemic forced educators to teach in an online environment. This was particularly challenging for those teaching courses that are intended to support bench science research. This practitioner article tells the story of how an instructor transformed their Course-based Undergraduate Research Experience (CURE) using the Backwards Design Method into a synchronous online course. Research objectives in this transformed course included: conducting a literature review, identifying research questions and hypotheses based on literature, and developing practical and appropriate research methodologies to test these hypotheses. We provide details on how assignments were created to walk students through the process of research study design and conclude with recommendations for the implementation of an online CURE. Recommendations made by the instructor include scaffolding the design, building opportunities for collaboration, and allowing students to fail in order to teach the value of iteration. The Backwards Design framework naturally lends itself to a scaffolded instructional approach. By identifying the learning objectives and final assessment, the learning activities can be designed to help students overcome difficult concepts by filling in the gaps with purposeful instruction and collaborative opportunities. This present course also practiced iteration through the extensive feedback offered by the instructor and opportunities for students to revise their work as their understanding deepened. Anecdotally, based on end of course reviews, students overall had a positive experience with this course. Future work will examine the efficacy of student learning in this online environment and is forthcoming.

Quantum biology studies span multiple disciplines including physics, engineering, and biology with the goal of understanding the quantum underpinnings of living systems. Recent findings have brought wide attention to the role of quantum mechanisms in the function and regulation of biological processes. Moreover, a number of activities have been integral in building a vibrant quantum biology community. Due to the inherent interdisciplinary nature of the field, it is a challenge for quantum biology researchers to integrate and advance findings across the physical and biological disciplines. Here we outline achievable approaches to developing a shared platform—including the establishment of standardized manipulation tools and sensors, and a common scientific lexicon. Building a shared community framework is also crucial for fostering robust interdisciplinary collaborations, enhancing knowledge sharing, and diversifying participation in quantum biology. A unified approach promises not only to deepen our understanding of biological systems at a quantum level but also to accelerate the frontiers of medical and technological innovations. [ABSTRACT FROM AUTHOR]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2006.08.046 Byline: Wendy S. Beane (a), Ekaterina Voronina (b), Gary M. Wessel (b), David R. McClay (a) Keywords: Ras GTPase; Rho; G protein; Galpha; Dynamin; SRP; Signal recognition particle receptor; Translation; Gene duplication; Phylogenomics; Echinoderm Abstract: In every organism, GTP-binding proteins control many aspects of cell signaling. Here, we examine in silico several GTPase families from the Strongylocentrotus purpuratus genome: the monomeric Ras superfamily, the heterotrimeric G proteins, the dynamin superfamily, the SRP/SR family, and the 'protein biosynthesis' translational GTPases. Identified were 174 GTPases, of which over 90% are expressed in the embryo as shown by tiling array and expressed sequence tag data. Phylogenomic comparisons restricted to Drosophila, Ciona, and humans (protostomes, urochordates, and vertebrates, respectively) revealed both common and unique elements in the expected composition of these families. G[alpha] and dynamin families contain vertebrate expansions, consistent with whole genome duplications, whereas SRP/SR and translational GTPases are highly conserved. Unexpectedly, Ras superfamily analyses revealed several large (5+) lineage-specific expansions in the sea urchin. For Rho, Rab, Arf, and Ras subfamilies, comparing total human gene numbers to the number of sea urchin genes with vertebrate orthologs suggests reduced genomic complexity in the sea urchin. However, gene duplications in the sea urchin increase overall numbers such that total sea urchin gene numbers approximate vertebrate gene numbers for each monomeric GTPase family. These findings suggest that lineage-specific expansions may be an important component of genomic evolution in signal transduction. Author Affiliation: (a) Department of Biology, Developmental, Cell and Molecular Group, Duke University, Box 91000, Durham, NC 27708, USA (b) Department of Molecular and Cell Biology and Biochemistry, Brown University, 69 Brown Street, Providence, RI 02912, USA Article History: Received 11 May 2006; Revised 18 August 2006; Accepted 19 August 2006

A study on the embryonic development of sea urchin examines the in-silico screening of the genome.

A study examines the protein kinases seen in the sea urchin kinome and compares them with the kinases found in human beings.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2005.12.031 Byline: Wendy S. Beane (a), Jeffrey M. Gross (b), David R. McClay (a) Keywords: Sea urchin; RhoA; Gastrulation; Invagination; Convergent extension; Brachyury Abstract: During gastrulation, the archenteron is formed using cell shape changes, cell rearrangements, filopodial extensions, and convergent extension movements to elongate and shape the nascent gut tube. How these events are coordinated remains unknown, although much has been learned from careful morphological examinations and molecular perturbations. This study reports that RhoA is necessary to trigger archenteron invagination in the sea urchin embryo. Inhibition of RhoA results in a failure to initiate invagination movements, while constitutively active RhoA induces precocious invagination of the archenteron, complete with the actin rearrangements and extracellular matrix secretions that normally accompany the onset of invagination. Although RhoA activity has been reported to control convergent extension movements in vertebrate embryos, experiments herein show that RhoA activity does not regulate convergent extension movements during sea urchin gastrulation. Instead, the results support the hypothesis that RhoA serves as a trigger to initiate invagination, and once initiation occurs, RhoA activity is no longer involved in subsequent gastrulation movements. Author Affiliation: (a) Department of Biology, Developmental, Cell and Molecular Group, Duke University, PO Box 91000, Durham, NC 27708, USA (b) Molecular Cell and Developmental Biology, University of Texas at Austin, 1 University Station A6700, Austin, TX 78712, USA Article History: Received 6 October 2005; Revised 6 December 2005; Accepted 14 December 2005

Amphibians such as frogs can restore lost organs during development, including the lens and tail. To design biomedical therapies for organ repair, it is necessary to develop a detailed understanding of natural regeneration. Recently, ion transport has been implicated as a functional regulator of regeneration. Whereas voltage-gated sodium channels play a well known and important role in propagating action potentials in excitable cells, we have identified a novel role in regeneration for the ion transport function mediated by the voltage-gated sodium channel, Nav1.2. A local, early increase in intracellular sodium is required for initiating regeneration following Xenopus laevis tail amputation, and molecular and pharmacological inhibition of sodium transport causes regenerative failure. Na~l .2 is absent under nonregenerative conditions, but misexpression of human Na~1.5 can rescue regeneration during these states. Remarkably, pharmacological induction of a transient sodium current is capable of restoring regeneration even after the forma- tion of a nonregenerative wound epithelium, confirming that it is the regulation of sodium transport that is critical for regenera- tion. Our studies reveal a previously undetected competency window in which cells retain their intrinsic regenerative program, identify a novel endogenous role for Na~ in regeneration, and show that modulation of sodium transport represents an exciting new approach to organ repair. [ABSTRACT FROM AUTHOR]

With the growth of the quantum biology field, the study of magnetic field (MF) effects on biological processes and their potential therapeutic applications has attracted much attention. However, most biologists lack the experience needed to construct an MF exposure apparatus on their own, no consensus standard exists for exposure methods, and protocols for model organisms are sorely lacking. We aim to provide those interested in entering the field with the ability to investigate static MF effects in their own research. This protocol covers how to design, build, calibrate, and operate a static MF exposure chamber (MagShield apparatus), with instructions on how to modify parameters to other specific needs. The MagShield apparatus is constructed of mu-metal (which blocks external MFs), allowing for the generation of experimentally controlled MFs via 3-axial Helmholtz coils. Precise manipulation of static field strengths across a physiologically relevant range is possible: nT hypomagnetic fields, μT to < 1 mT weak MFs, and moderate MFs of several mT. An integrated mu-metal partition enables different control and experimental field strengths to run simultaneously. We demonstrate (with example results) how to use the MagShield apparatus with Xenopus , planarians, and fibroblast/fibrosarcoma cell lines, discussing the modifications needed for cell culture systems; however, the apparatus is easily adaptable to zebrafish, C. elegans , and 3D organoids. The operational methodology provided ensures uniform and reproducible results, affording the means for rigorous examination of static MF effects. Thus, this protocol is a valuable resource for investigators seeking to explore the intricate interplay between MFs and living organisms. Key features • A comprehensive roadmap, suitable for undergraduate to advanced researchers, to construct an apparatus for in vitro and in vivo experiments within uniform static magnetic fields. • Designed to fit inside standard incubators to accommodate specific environmental conditions, such as with cell culture, in addition to stand-alone operation at room temperature. • Requires two DC power supplies and 3D printer access for the Helmholtz coils, Plexiglass and mu-metal foil for the partition, and a milli/Gaussmeter for calibration. • Requires ordering a custom mu-metal shell from a commercial resource (using provided schematics), where lead times for delivery can vary from 2 to 4 months., Competing Interests: Competing interestsThe authors confirm that there are no competing interests., (©Copyright : © 2024 The Authors; This is an open access article under the CC BY-NC license.)

Amphibians such as frogs can restore lost organs during development, including the lens and tail. To design biomedical therapies for organ repair, it is necessary to develop a detailed understanding of natural regeneration. Recently, ion transport has been implicated as a functional regulator of regeneration. Whereas voltage-gated sodium channels play a well known and important role in propagating action potentials in excitable cells, we have identified a novel role in regeneration for the ion transport function mediated by the voltage-gated sodium channel, Na(V)1.2. A local, early increase in intracellular sodium is required for initiating regeneration following Xenopus laevis tail amputation, and molecular and pharmacological inhibition of sodium transport causes regenerative failure. Na(V)1.2 is absent under nonregenerative conditions, but misexpression of human Na(V)1.5 can rescue regeneration during these states. Remarkably, pharmacological induction of a transient sodium current is capable of restoring regeneration even after the formation of a nonregenerative wound epithelium, confirming that it is the regulation of sodium transport that is critical for regeneration. Our studies reveal a previously undetected competency window in which cells retain their intrinsic regenerative program, identify a novel endogenous role for Na(V) in regeneration, and show that modulation of sodium transport represents an exciting new approach to organ repair.