bluuebunny/crossref_metadata_2025_split huggingface dataset:
Redesign of Introductory Biology Courses to Align with Vision and Change Recommendations Improves Student Success
Authors: Wilkinson Katherine A. , Anand Sulekha , Lambrecht Susan 
Published: June 2021

The SJSU Biological Sciences Department recently redesigned the core introductory biology sequence to align with the best practices in biology pedagogy as described in the Vision and Change in Undergraduate Biology Education report. We now emphasize depth not breadth of information and focus on understanding how to interpret experimental results. We have incorporated more inquiry‐based labs and active learning strategies, including out of class reading quizzes and in‐class clicker questions. Our goal is to improve student performance in this 2 semester‐long lecture and lab course and improve student preparation for success in the major. To assess the success of our redesign and aid in our understanding of the student population that takes these courses, we administer two validated concept inventories, the Biology Concept Inventory (BCI)and the Test of Scientific Literacy Skills (TOSLS), and a demographic survey at the beginning of the first course and the end of the second course. We have finished the first full year of the redesigned series and have seen modest improvements in failure rates (old version: BIOL 1A: 22%, BIOL 1B: 24% failure rate; new version: BIOL 30: 19%, BIOL 31: 13%). We also saw improvements in the performance of first generation college students and students from underrepresented minority groups in the new courses as well as increased retention into the second semester. Students in both versions of the courses scored significantly higher on the BCI following the second semester, suggesting improved mastery of the course content. Students in the old version of the course scored significantly worse on the TOSLS in the second semester, while students in the new version of the course had post‐test TOSLS scores that were trending higher, suggesting the new version was more effective in improving scientific literacy skills. We are continuing to track student success in future courses and are investigating changes in student attitudes about science with the Colorado Learning Attitudes about Science Survey (CLASS). Overall, the redesign has had positive effects on student success.Support or Funding InformationWe are supported by a California State University Program in Education and Research in Biotechnology (CSUPERB) Curriculum Grant.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Evolutionary Developmental Biology (Evo‐Devo‐Path), or Macroevolutionary Medicine: linking anatomy, evolution, development and human pathologies
Authors: Diogo Rui 
Published: June 2021

Since the rise of Evo‐Devo in the 1980s few authors have attempted to combine the increasing knowledge obtained from the study of model organisms and human medicine with data from comparative and evolutionary biology in order to investigate the links between development, pathology and macroevolution. Fortunately, this situation is slowly changing, with a renewed interest in Evolutionary Developmental Pathology (Evo‐Devo‐Path) in the last decades. However, this interest and the new data obtained from it, as well as their main implications for evolution and medicine, have not been the object of a synthesis to the broader scientific community and wider public. In this talk I will thus provide such a synthesis. Specifically, I will provide a brief historical account on the study of the links between evolution, development and pathologies, followed by case studies from the recent work done by me and other colleagues on subjects related to Evo‐Devo‐Path, and then by a general discussion on the broader anatomical, developmental and macroevolutionary implications of these case studies and of research recently done by other authors. An important component is to therefore also contribute to the understanding of the links between the phenotype and the genotype, within both normal and abnormal development. Therefore I will also include the results of work I have been doing with physicians and surgeons who are interested in directly applying and/or collecting Evo‐Devo‐Path data to their own medical interventions, as part of an effort to focus on the applications and implications of these data for direct medical use. My primary aim is to highlight the strength of studying developmental anomalies within an evolutionary framework to understand morphological diversity and disease by connecting these recent works with the research done and broader ideas proposed by authors such as Étienne Geoffroy Saint‐Hilaire, Waddington, Goldschmidt, Gould and Per Alberch, among many others, to pave the way for further and much needed work regarding abnormal development and macroevolution.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Shaping the craniofacial skeleton of Mexican cavefish (Astyanax mexicanus); Role of Osteoblast and Osteoclast
Authors: Atukorallaya Devi Sewvandini Atukorala , Ratnayake Ravindra Kumar 
Published: June 2021

The vertebrate bony skeleton is remodelled continuously by bone deposition and reabsorption, which is essential for normal development, growth, repair and for the mineral homeostasis. Remodelling of the skeleton usually involves the removal of the bone by osteoclasts and the subsequent formation of new bone by osteoblasts. These remodelling mechanisms can be found in the teleost fish skeleton with special adaptation to the aquatic life. Most of the fish species have teeth in their craniofacial region and replace their dentitions though out the life which lead to continuous bone remodelling activity in the tooth‐bearing bones. The Mexican tetra (Astyanax mexicanus), is a small teleost fish that exists as two morphs; sighted and blind cave form. The degeneration of the eyes, result in the characteristics craniofacial phenotype in cavefish. However, little is known about the cellular mechanisms underlying the remodelling activity of the skeleton of this species. This study was designed to identify the cellular interactions during the development of craniofacial skeleton of Mexican cavefish. Histological and whole mount analysis was performed to compare the development of the skeleton in these two morphs. The cavefish showed delayed eruption of teeth in tooth‐bearing bones but has large jaw bones compared to the surface larval fish. Sites of bone resorption in the bony skeleton will be investigated by RNA in situ hybridization and ultrastructural analysis. Live bone staining techniques will be used to identify the pattern of bone deposition. This study will provide insights into the evolution of osteoblastic and osteoclastic cell activity and will highlight the use of this species as a model in mammalian skeletal disorders.Support or Funding InformationThis research was funded by the University of Manitoba.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Temporal Effect of Hydrocortisone Treatment on Conjunctival Papillae in the Chicken Eye
Authors: Drake Paige M. , Franz‐Odendaal Tamara A. 
Published: June 2021

Intramembranous ossification is still poorly understood. Chicken embryos (Gallus gallus) have served as excellent models for investigating bone development. Scleral ossicles are a series of 13–15 bones that overlap to constitute a single sclerotic ring of bone. They have no articulation with the skull and are positioned in the corneal‐scleral limbus of the eye. The scleral ossicles are ideal elements in which to investigate the developmental processes underlying intramembranous ossification, as they are easily accessible for embryonic manipulations. Each ossicle is induced by corresponding regions of thickened epithelia called conjunctival papillae. The cells below the papillae ultimately differentiate into osteoblasts and deposit bone matrix. Research in the past decade has examined various factors that affect ossicle development, such as bone morphogenetic protein (BMP) and hedgehog (HH) signalling pathways, hydrocortisone treatment, vasculature, and vascular endothelial‐derived growth factor (VEGF) expression. The objective of this research is to further elucidate the mechanism by which hydrocortisone affects the development of scleral papillae. Here we explore the precise timing of hydrocortisone injections that is sufficient to inhibit the formation of all scleral papillae. Our previous research showed that delivering hydrocortisone injections at HH29 and HH30 produced the most significant effects on scleral condensation morphology and number. By adjusting the injection time points by an hour in each experiment, we determined the ideal window when hydrocortisone injections are sufficient to completely disrupt all papillae in 100 % of the injected embryos. For example, delivering the injections 18 hours apart results in the prevention of 12/13 conjunctival papillae in 100% of the embryos (n=4). This result indicates signalling mechanisms responsible for inducing conjunctival papillae are likely active almost a full day prior to the first papilla becoming morphologically visible at HH29. This study has implications for future research towards elucidating the genetic mechanisms underlying conjunctival papillae development.Support or Funding InformationThis research was funded by the Natural Sciences and Engineering Research Council of Canada.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Critical Roles of Rostral‐Process‐Meckel's‐Cartilage in Mandibular Formation and Repairing
Authors: Jing Yan , Li Chaoyuan , Zhao Hu , Feng Jian 
Published: June 2021

ObjectivesIt is generally accepted that mandibular ossification and regeneration occur via an intramembranous mechanism; and that mandible cartilage is associated but does not directly contribute to bone formation. The goal of this study was to investigate whether and how Rostral Process (RP)‐Meckel's cartilage (MC) directly contributes to mandibular growth and repair.MethodsTo define the cell fate of mouse MC, R26RTomato mice were separately crossed with inducible Gli1‐CreERT2 (expressed in early progenitor cells), Aggrecan‐CreERT2 (Acan, expressed in all cartilage), or Col10a1‐Cre (expressed in hypertrophic chondrocytes) mice, with or without 2.3Col1a1‐GFP (expressed in bone cells). Mice were sacrificed from E11.5 (before Meckel's cartilage) to P28. The combined approaches of in vivo cell lineage‐tracing, histology, confocal microscopy, and immunohistochemistry with different cartilage and bone markers were used to determine the contributions of cartilage in mandibular development and repair.ResultsThe first sign of intramembranous bone was observed at E13.5 along the mandible dentary. From E15.5, numerous MC‐derived bone cells clearly presented with bone markers expression, such as Col I and DMP1, indicating a direct transformation of MC chondrocytes into bone cells in both Col10a1‐Cre and Acan‐CreERT2 background. Importantly, a separate progenitor niche (Gli1+ and Acan+, named condensed mesenchymal progenitor, CMP) was identified. Further studies showed that CMPs are responsible for the formation of the RP and expansion of MC during postnatal mandibular growth. In a trauma response, we clearly demonstrated both chondrocyte‐derived and non‐chondrocyte derived bone cells take part in bone repairing.Conclusions1) The mandibular bone originates from non‐cartilage‐derived and cartilage‐derived bone cells; 2) The CMP‐RP‐MC, equivalent to a long bone growth plate, is responsible for expansion of the anterior portion of the mandible, including symphysis; and 3) both chondrocyte‐derived and non‐chondrocyte‐derived bone cells coordinate for mandibular bone repairing. This work sheds new light on the mandibular development and repair process.Support or Funding InformationNIH DE025659 to JQF; Burstone□Indiana Biomechanics Award (AAOF) to YJThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
A new transgenic Xenopus reporter line reveals dynamic expression of snail2 during cranial neural crest development
Authors: Makhija Aditi , Li Jiejing , Perfetto Mark , Wang Jian , Shah Anoop , Tran Hong Thi , Vleminckx Kris , Wei Shuo 
Published: June 2021

During vertebrate embryogenesis, the cranial neural crest (CNC) is induced at the neural plate border (NPB) and subsequently migrate and differentiate into various cells and tissues. In Xenopus, the transcription factor Snail2 is induced at the NPB by canonical Wnt signaling and is required for CNC induction and migration, but the roles of Snail2 at later stages remain unclear. To monitor CNC development in live embryos, we generated a transgenic X. tropicalis line expressing Green Fluorescent Protein(GFP) driven by the snail2 promoter. Using whole‐genome sequencing, we mapped the transgene insertion to a noncoding region. Live imaging of the transgenic embryos reveals that snail2 is expressed in pre‐migratory and migrating CNC but is lost in CNC cells that have arrived at their destinations. However, snail2 is re‐expressed during CNC differentiation in all CNC derivatives that were examined. Defects in CNC differentiation, in addition to induction and migration, can be readily detected using this transgenic snail2 reporter line. Finally, comparison with a transgenic Wnt reporter line shows that Wnt signaling is consistently activated prior to snail2 expression, suggesting that the Wnt‐Snail2 axis may play important roles in multiple stages of CNC development. We are also developing a new transgenic line with a photoconvertible protein instead of GFP that can be used to monitor cell fate of various CNC branches for lineage tracing of CNC derivatives.Support or Funding InformationFunded by: NIH DE022813 and GM114105This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Hox Regulation of Neural Crest Cells during Craniofacial Development
Authors: Pushel Irina , Krumlauf Robb 
Published: June 2021

Craniofacial structures are shaped by the formation, migration, and differentiation of cranial neural crest cells (cNCCs) in the developing embryo. Many craniofacial defects are caused by misregulation in this embryonic cell population. Recent work has identified key components of the gene regulatory network (GRN) responsible for cNCC development, but there remain gaps in our knowledge. One such example is the Hox family of genes, which are known to pattern subsets of cNCCs and show jaw, ear, and palate defects when misexpressed, yet whose role in the GRN remains unknown. We study mouse embryogenesis to identify which factors Hox genes regulate throughout cNCC development and determine the mechanism by which they contribute to the identity of cNCC derivatives. To approach this question, we use RNAseq to compare the transcriptomes of Hox‐positive and Hox‐negative cNCCs and generate a candidate list of genes that are potential Hox targets. We identified several genes known to be involved in the cNCC GRN, allowing us to begin integrating the Hox genes into this network, as well as novel targets that appear to be significant in craniofacial development. To identify the regulatory mechanisms that affect Hox targets, we use ATAC‐seq to compare chromatin accessibility between cNCC subpopulations and identify enhancers that may modulate the expression of genes downstream of the Hox family. We are working to systematically test the more promising targets through perturbation, expression analysis in mutants, and reporter assays to validate direct regulatory interactions between Hox genes and other key factors of the GRN, particularly as they relate to differences between subpopulations of cNCCs that give rise to distinct derivatives. Expanding current knowledge of the GRN governing cNCC development in this manner establishes a greater foundation for future work on this cell population. Moreover, the integration of the Hox genes, as one specific example, into this framework will develop a more precise understanding of the developmental dynamics responsible for craniofacial defects and can ultimately inform clinical approaches to the etiology and treatment of these defects.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Connexin 43 Function in the Cranial Neural Crest
Authors: Jourdeuil Karyn , Taneyhill Lisa A. 
Published: June 2021

Connexins are transmembrane proteins that cluster to form intercellular channels called gap junctions, which function to allow direct diffusion of small molecules and ions between adjacent cells. Gap junctions are composed of two connexons (one on each cell which are docked head‐to‐head) consisting either of homomeric or heteromeric connexin proteins, although only certain combinations of connexins are possible. Connexin 43 is one of the predominant components of gap junctions and is expressed in multiple organisms and their tissues. To date, however, very little is known about the role of gap junctions, and specifically Connexin 43, in the neural crest. Immunohistochemical analyses revealed that Connexin 43 is expressed in premigratory cranial neural crest cells as well as during the epithelial‐to‐mesenchymal transition (EMT), migration, and coalescence of neural crest cells with placodal neurons as the trigeminal ganglion assembles. Interestingly, Connexin 43 is also observed in the cranial mesenchyme, but placodal neurons lack Connexin 43. Given the robust expression of Connexin 43 in the neural crest, we sought to elucidate the role of Connexin 43, and gap junctions in particular, during neural crest cell EMT and migration. To this end, we are assessing the presence of gap junctions in the neural crest and performing molecular and chemical perturbation experiments to alter Connexin 43 and general gap junction function. Our initial results reveal that gap junctions form between migratory neural crest cells generated from explants of premigratory neural crest tissue in an ex vivo culture assay. In future experiments, we will inhibit gap junctions using pharmacological reagents and modulate levels of Connexin 43 through knockdown and overexpression experiments, evaluating effects on neural crest cell EMT and migration in all approaches. Importantly, these assays will confirm that Connexin 43 is critical for gap junction function in neural crest cells. These data will provide insight into how neural crest cells interact and communicate during EMT and migration to allow for proper embryonic patterning throughout vertebrate development.Support or Funding InformationThis research was funded by ACS RSG‐1502301‐CSM and NIH R01DE024217 (L.A.T.).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
TMED2 is Required in both the Chorion and Placenta for Placental Labyrinth Layer Development
Authors: Jerome‐Majewska Loydie , Hou Wenyang 
Published: June 2021

The transmembrane emp24 domain/p24 (TMED) family are essential components of the vesicular transport machinery. TMED family members serve as cargo receptors important for selection and packaging of endoplasmic reticulum (ER) luminal proteins into coatomer (COP) II coated vesicles for anterograde transport to the Golgi. Until recently the role of TMED proteins in development and disease remained a mystery. We postulated that members of the TMED family regulate transport of cargo proteins essential for normal development and homeostasis. Tmed2, the sole member of the vertebrate Tmed β‐subfamily, shows tissue and temporal specific patterns of expression during embryogenesis, but is ubiquitously expressed in all adult organs. We previously showed that mouse embryos homozygous mutant for a single point mutation, the 99J mutation, in the signal sequence of Tmed2 fail to form a functional placenta, and that heterozygous mice carrying this mutation developed non‐alcoholic liver disease. Using explants of chorion and allantois, the precursors of the developing placenta, we identified several secreted and membrane‐bound proteins that were abnormally expressed in Tmed2 mutant tissues, indicating a role for TMED2 in transport of secreted and membrane bound cargoes. In addition, explants between wild type chorion and Tmed2 homozygous mutant allantois, and vice‐versa, revealed both cell‐non‐autonomous and cell‐autonomous requirements for TMED2 during placental development. Our studies indicate that TMED2 is required for organogenesis of the placenta, which, is essential for survival of the growing fetus.Support or Funding InformationNatural Sciences and Engineering Research CouncilThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Does Stature Really Matter? The Effect of Short Stature on Adult Survivorship
Authors: Minsky‐Rowland Jocelyn D. 
Published: June 2021

Stature is a multifactorial growth process, influenced by genetics, health and nutrition. Short stature estimates from skeletal remains have traditionally been used as an indicator of a disruption in physiological growth processes within past populations, which may decrease adult survivorship. This project questions whether this non‐specific indicator of stress, affected the survivorship of individuals associated with the historic Arikara Native Americans of South Dakota (AD 1600–1832). Previous research suggests that short stature decreased survivorship among adult individuals from one archaeological site. In that study, the two sexes were pooled and survivorship was estimated relative to different time periods. In the current project, survivorship differences between the sexes were estimated, while time period was pooled. It is hypothesized that individuals with below average stature will exhibit a decrease in survivorship compared to their taller peers. One‐hundred and eighty‐four adult individuals, (79 females, 105 males), across four archaeological sites, were analyzed. Survivorship was estimated using Kaplan‐Meier estimates with log‐rank tests in SPSS version 22. Two analytical steps were taken. First, differences in survivorship between tall and short individuals were estimated per sex. Next, survivorship of tall females and tall males was compared and survivorship of short females and short males was compared. The results were not statistically significant. Therefore, short stature does not affect survivorship relative to sex. Broadly, these results suggest that the significance of short stature is context specific and cannot always be used as an indicator of decreased survivorship. It is recommended that researchers utilize multiple indicators of stress to infer survivorship and health in past populations. This project contributes to research focused on human growth, the disruption of physiological processes and their effects on adult survivorship.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.