A strong understanding of distinct gene components and the ability to retrieve relevant information from gene databases are necessary to answer a diverse set of biological questions. However, often there is a considerable gap between students’ theoretical understanding of gene structure and applying that knowledge to design laboratory experiments. In order to bridge that gap, our lesson focuses on how to take advantage of readily available gene databases, after providing students with a strong foundation in the central dogma and gene structure. Our instructor-led group activity aids students in navigating the gene databases on their own, which enables them to design experiments and predict their outcomes. While our class focuses on cardiomyocyte differentiation, classes with a different focus can easily adapt our lesson, which can be conducted within a single class period. Our lesson elicits high engagement and learning outcomes from students, who gain a deeper understanding of the central dogma and apply that knowledge to studying gene functions

The rapidly evolving stem cell field puts much stress on developing educational resources. The ISSCR Education Committee has created a flexible stem cell syllabus rooted in core concepts to facilitate stem cell literacy. The free syllabus will be updated regularly to maintain accuracy and relevance.

ABSTRACT We assessed the efficacy of traditional lectures versus online modules with respect to student learning in an undergraduate introductory biochemistry course in two successive years. In the first year, students had the options of attending live lectures by the course instructor and viewing online modules pre-recorded by the instructor, with the lectures and modules covering identical content; in addition, all students had a mandatory weekly application session. Utilizing pre-course and post-course tests as an instrument with which to measure learning during the course, we observed significantly increased learning (0.7 standard deviations) with attendance of traditional lectures and decreased learning with use of online modules, even after adjustment for grade point average. In the second year, the course had the same curriculum, but students were randomized to either live lectures or online modules for the first half of the course, crossing over to the other modality during the second half. With randomization, no difference in learning was observed between the two groups. Furthermore, we found that students self-reported greater engagement when viewing online modules than when attending lectures in person. These findings suggest some aspects of the lecture experience can be shifted to online modules in STEM courses without impacts on student learning so as to use classroom time more fully for application-based active learning interventions.

The COVID-19 global pandemic has forced the higher education sector to transition to an uncharted remote-learning format. This offers an opportunity to adopt active learning, which increases students' performance compared to lectures, narrows achievement gaps for underrepresented students, and promotes equity and inclusivity, as the basis of STEM education.

Teaching positions provide a rewarding career pathway for Ph.D.s wishing to stay in academia outside of the research-focused position. The balance of teaching and research expectations on faculty can vary greatly depending on the type of institution. Faculty at primarily undergraduate institutions may be required to be researchactive and mentor undergraduates in the laboratory, while teaching faculty at a research-centered university may not have a research lab. In addition, faculty are expected to actively contribute to the shared governance of the institution, in the name of service. The career in teaching has become highly competitive and offers unexpected rewards and benefits. Considered here are the differences found among teaching positions to serve as a guide when considering teaching as a career option. We include our personal career narratives to illustrate the driving forces that led each of us to this challenging yet fulfilling academic path.

Manipulating gene expression is a commonly used tool to study the effect of a single gene or the hierarchy of gene networks in many different biological disciplines. When working with mice, the most commonly used techniques to manipulate genes include gene targeting via homologous recombination to achieve loss-of-function and gain-of-function mutations. Students often struggle with the concepts behind homologous recombination and the physical changes that happen at the target gene locus. Our activity uses different colored ribbons connected by hook-and-loop fasteners (e.g., those most popularly produced by the VELCRO Brand) that students use to design targeting constructs as well as to model the recombination between their constructs and the gene locus. This hands-on exercise helps students better understand the mechanisms of homologous recombination happening at the gene locus, enabling them to progress to higher-level cognition such as predicting experimental outcomes and designing their own gene targeting experiments.

When they were students, many current science instructors learned through traditional lectures. This mode of passive knowledge transmission has been shown to be less effective for student learning than an approach that involves students in a more active and engaged role in their learning. Without first-hand experiences with active learning, current instructors face challenges as they try to incorporate active learning experiences into their classrooms. In this review, we summarize the field of active learning, including relevant pedagogical philosophy and features of commonly used activities. We end with future considerations that could help disseminate and improve the implementation of active learning in college science classes.

One of the challenges of teaching Cell Biology is helping students understand important research methods used to study cells. The goal of understanding cell biology methods is especially challenging in courses without a laboratory component. When studying cells, determining the location of a protein is important for understanding the protein's cellular function. In this lesson, upper-division Cell Biology students will learn about two commonly used methods for protein localization: 1) immunoblotting after differential centrifugation, and 2) immunofluorescence microscopy. They will work in small groups to answer questions in a problem set written in the spirit of Process-Oriented Guided Inquiry Learning (POGIL). Students will explore key points of the two methods and then apply their knowledge to the analysis of protein localization data from the primary literature. Analyzing protein localization data will help students develop the ability to “apply the process of science”, which is one of the Vision and Change core competencies.

Scientists constantly make groundbreaking discoveries, some of which receive attention from the press. We designed a course intended for a lay audience that provides the scientific background to appreciate these reports more fully. We discuss three topics in the life sciences: stem cells, cancer, and infectious disease. The course is structured to blend relevant scientific background and evaluation of primary literature with the coverage of these advances by the media and popular press. In short, lectures emphasize exposure to basic biological concepts and tools as a means of informing understanding of prominent biological questions of public interest. The overall goal of the course is not only to expose students to the media’s coverage of scientific progress, but also to hone their critical thinking skills to distinguish hope from hype.

Most scientific research is judged based on the quality of controlled experiments and carefully analyzed results. In addition, proper levels of regulation in terms of biosafety and animal usage are a routine part of the scientific research process for laboratories. For many biologists, educational research is much more of a black box. While faculty have many great ideas on how to improve education, they struggle with the best way to evaluate whether their ideas lead to greater student outcomes. Here we provide a review of compliance issues related to educational research, as well as describe ways in which pedagogical innovations in biology can be assessed. We also describe some of the challenges related to educational research and how these could be addressed.

Chondroitin sulfate proteoglycans (CSPGs) are known to be deposited in high concentrations near regions of neural injury. They are also believed to play a role in the inhibition of neural regeneration and axonal growth, which can be lessened to a degree by enzyme digestion of the chondroitin sulfate (CS) side chains. Shen et al now also demonstrate a neural specific receptor, the transmembrane protein tyrosine phosphatase, PTPσ, which binds with high affinity to the chondroitin sulfate side chains on CSPGs. The binding location involves the extracellular first immunoglobulin-like domain on the PTPσ receptor. The authors demonstrate cultured PTPσ−/− neurons that have reduced growth inhibition by CSPG. Additionally, and perhaps useful therapeutically, Shen et al. were able to create a membrane free PTPσ fusion protein probe, capable of demonstrating proteoglycans in injured regions. The authors point out that identification of a specific CSPG receptor is helpful from a pathophysiology viewpoint, since previously it has been hypothesized that the inhibition of neural regrowth secondary to these molecules involved nonspecific mechanisms. The PTP family has known affinity for heparin sulfate proteoglycans, and seem to play a role in axon guidance in development. In this work, Shen et al performed a binding assay between a free recombinant fusion version of the receptor (PTPσ-Fc) with neurocan (one of the dominant CSPGs found in neural injury sites). The binding showed saturability and high affinity, with a binding constant (KD) of 11 nM, a value within the typically measured range of cellular receptors. Using assays pretreated with chondroitin-sulfate-ABC endolyase eliminated most of the binding between CSPGs and the fusion PTPσ-Fc molecule, indicating that the chondroitin sulfate side chain moieties play the primary role in binding. This also indicates likely strong affinity for other CSPGs produced by astrocytes after neural injury, including neurocan and aggrecan as tested in this effort. Shen et al. also explored the growth patterns of cultured neurons derived from PTPσ−/− mice in the presence of mixed neural CSPG solutions and purified neurocan. These CSPG solutions had much less of an effect on neuritic outgrowth from the PTPσ−/− neurons compared to controls. Some inhibitory effects stilled remained however, indicating the possible activity of other receptor-dependent or independent growth inhibition mechanisms. Shen et al. additionally demonstrate the specific affinity of the PTPσ-Fc fusion molecule for injured spinal cord locations, at one week after injury in a mouse injury model (Figure). The labeling provided by the fusion molecule overlapped labeling for the CSPG neurocan, and demonstrates promise for an assay to detect the locations of neural injury. The authors were also able to perform an in vivo post-injury growth assessment by using a spinal cord injury model based on PTPσ−/− mice. In these mice, axonal growth into the lesion after injury was significantly improved compared to wild-type mice. Axonal extension was never complete, however, through the injury sites, perhaps indicating the function of other receptor-based or nonspecific inhibitory actors. In summary, Shen et al. point out that the specific neuron based cell surface receptor (PTPσ) which has a high affinity for chondroitin sulfate proteoglycans may have therapeutic promise as a target to block during efforts to promote neural regeneration, and might also prove useful as a probe for neural injury.FIGURE: Using the PTPσ fusion protein for CSPG detection at spinal cord injury sites. Specimens double-stained with antibody to neurocan (Ncn, red) and either PTPσ–Fc probe (green) or Fc control (green). A, unlesioned spinal cord, no significant PTPσ–Fc labeling above controls. B, spinal cord specimens, 7 days after injury. Lesion site shows increases in neurocan labeling and roughly overlapping PTPσ–Fc binding.WILLIAM S. ANDERSON

The airways are conduits that transport atmospheric oxygen to the distal alveolus. Normally, airway mucous cells are rare. However, diseases of the airway are often characterized by mucous metaplasia, in which there are dramatic increases in mucous cell numbers. As the Notch pathway is known to regulate cell fate in many contexts, we misexpressed the active intracellular domain of the mouse Notch1 receptor in lung epithelium. Notch misexpression resulted in an increase in mucous cells and a decrease in ciliated cells in the airway. Similarly, mouse embryonic tracheal explants and adult human airway epithelium treated with Notch agonists displayed increased mucous cell numbers and decreased ciliated cell numbers. Notch antagonists had the opposite effect. Notably, Notch antagonists blocked IL13-induced mucous metaplasia. IL13 has a well-established role as an inflammatory mediator of mucous metaplasia and functions through Stat6-mediated gene transcription. We found that Notch ligands, however, are able to cause mucous metaplasia in Stat6-null cultured trachea, thus identifying a novel pathway that stimulates mucous metaplasia. Notch signaling may therefore play an important role in airway disease and, by extension, Notch antagonists may have therapeutic value. Conversely, in the distal lung, Notch misexpression prevented the differentiation of alveolar cell types. Instead, the distal lung formed cysts composed of cells that were devoid of alveolar markers but that expressed some, but not all, markers of proximal airway epithelium. Occasional distal cystic cells appeared to differentiate into normal proximal airway cells, suggesting that ectopic Notch signaling arrests the normal differentiation of distal lung progenitors before they initiate an alveolar program.

The effects of Wnt7b on lung development were examined using a conditional Wnt7b-null mouse. Wnt7b-null lungs are markedly hypoplastic, yet display largely normal patterning and cell differentiation. In contrast to findings in prior hypomorphic Wnt7b models, we find decreased replication of both developing epithelium and mesenchyme, without abnormalities of vascular smooth muscle development. We further demonstrate that Wnt7b signals to neighboring cells to activate both autocrine and paracrine canonical Wnt signaling cascades. In contrast to results from hypomorphic models, we show that Wnt7b modulates several important signaling pathways in the lung. Together, these cascades result in the coordinated proliferation of adjacent epithelial and mesenchymal cells to stimulate organ growth with few alterations in differentiation and patterning.

A full description of the ontogeny of the β cell would guide efforts to generate β cells from embryonic stem cells (ESCs). The first step requires an understanding of definitive endoderm: the genes and signals responsible for its specification, proliferation, and patterning. This report describes a global marker of definitive endoderm, Claudin‐6 (Cldn6). We report its expression in early development with particular attention to definitive endoderm derivatives. To create a genetic system to drive gene expression throughout the definitive endoderm with both spatial and temporal control, we target the endogenous locus with an inducible Cre recombinase (Cre‐ER T2 ) cassette. Cldn6 null mice are viable and fertile with no obvious phenotypic abnormalities. We also report a lineage analysis of the fate of Cldn6 ‐expressing embryonic cells, which is relevant to the development of the pancreas, lung, and liver. Developmental Dynamics 237:504–512, 2008. © 2008 Wiley‐Liss, Inc.

1. Rajagopal et al. 2008. Development doi:10.1242/dev.015495 [OpenUrl][1][Abstract/FREE Full Text][2] [1]: {openurl}?query=rft.jtitle%253DDevelopment%26rft_id%253Dinfo%253Adoi%252F10.1242%252Fdev.015495%26rft_id%253Dinfo%253Apmid%252F18367557%26rft.genre%253Darticle%26rft_val_fmt%

The mammalian pancreas is constructed during embryogenesis by multipotent progenitors, the identity and function of which remain poorly understood. We performed genome-wide transcription factor expression analysis of the developing pancreas to identify gene expression domains that may represent distinct progenitor cell populations. Five discrete domains were discovered. Genetic lineage-tracing experiments demonstrate that one specific domain, located at the tip of the branching pancreatic tree, contains multipotent progenitors that produce exocrine, endocrine, and duct cells in vivo. These multipotent progenitors are Pdx1(+)Ptf1a(+)cMyc(High)Cpa1(+) and negative for differentiated lineage markers. The outgrowth of multipotent tip cells leaves behind differentiated progeny that form the trunk of the branches. These findings define a multipotent compartment within the developing pancreas and suggest a model of how branching is coordinated with cell type specification. In addition, this comprehensive analysis of >1,100 transcription factors identified genes that are likely to control critical decisions in pancreas development and disease.

Diurnal temperature range in winter wheat–growing regions of China: CMIP6 model evaluation and comparison,

The relative sizes of individual telomeres in cultured human cells under conditions of cell cycling, replicative quiescence, cell transformation and immortalization were determined using quantitative fluorescence in situ hybridization (Q-FISH) with a telomere-specific peptide nucleic acid (PNA) probe. Results obtained from analysis of telomere length profiles (TLPs), which display the distribution of relative telomere lengths for individual cells, confirmed telomere length heterogeneity at the single cell level and proportional shortening of telomere length during replicative aging of virus-transformed cells. TLPs also revealed that some telomeric ends of chromosomes are so closely juxtaposed within interphase nuclei that their fluorescent signals appear as a single spot. These telomeric associations (TAs) were far more prevalent in interphase nuclei of noncycling normal and virus-transformed cells than in their cycling counterparts. The number of interphase TAs per nucleus observed in late-passage E6/E7-transformed cells did not increase during progression to crisis, suggesting that telomere shortening does not increase the frequency of interphase TAs. Furthermore, interphase TAs were rarely observed in rapidly cycling, telomerase-positive, immortalized cells that exhibit somewhat shortened, but stabilized, telomere length through the activity of telomerase. Our overall results suggest that the number of interphase TAs is dependent more on whether or not cells are cycling than on telomere length, with TAs being most prominent in the nuclei of replicatively quiescent cells in which nonrandom (even preferred) chromosome spatial arrangements have been observed. We propose that interphase TAs may play a role in the generation and/or maintenance of nuclear architecture and chromosome positional stability in interphase nuclei, especially in cells with a prolonged G(1)/G(0) phase and possibly in terminally differentiated cells.

Many investigations have sought to determine the effect of lead exposure on the development of the cerebellum. This study addresses the effects of postnatal lead exposure in kittens on dendritic development of Purkinje cells. Golgi-Cox filled cells were used to measure dendritic branching patterns, spine density, height, width and distance from the cerebellar surface. The results revealed a significant increase in spine density and altered patterns of dendritic branching. Complex dendritic branching was evident with a progressive shift in peak branching peripherally. Lead-exposed Purkinje cells showed early sprouting with subsequent pruning. At 5 weeks of age dendritic branches on experimental cells were increased along the entire dendritic extent. Control Purkinje cells showed initial sprouting with subsequent pruning. Normal developmental growth spurts and lead-induced effects were evident on dendritic height, width and distance from the surface. Cerebella stained with hematoxylin and eosin and cresyl violet acetate showed no evidence of vascular damage or other pathologies. These findings corroborate the evidence of hyperspiny dendritic formation representing an important mechanism of neuronal plasticity. In regard to morphological effects of lead on rodents, the hyperspiny Purkinje cell dendrites and patterns of dendritic growth in lead-treated kittens offer an alternative interpretation of neurobehavioral findings of lead-burdened children. The results are discussed with reference to other aspects of lead exposure and neural development.