bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expanding Opportunities for Undergraduate Research: CUREs and Beyond
Authors: Teter Ken , Moore Sean , Borgon Robert A , Schneider Kimberly , Fedorka Ken 
Published: June 2021

The University of Central Florida (UCF) hosts over 2,500 students majoring in Biology, Biotechnology, or Biomedical Sciences. About half of these students have transferred to UCF from the state college system. To expand research opportunities for both transfer students and first time in college students, UCF has developed several research programs and curriculum‐based undergraduate research experiences (CUREs). The Transfer‐student Research and Integration Program (TRIP) prepares life science students for placement in graduate school or the STEM workforce by supporting their professional development and integration into the UCF community. TRIP students also receive a team‐based research experience in the form of Group‐Effort Applied Research (GEAR), a CURE that delivers concept‐driven lecture material and provides hands‐on training in the context of an active research project from the instructor's laboratory. Other CUREs at UCF include Applied and Industrial Microbiology (AIM) and Peer Instruction and Laboratory Occupational Training (PILOT). AIM provides interdisciplinary research experiences that are collaboratively linked to regional industries that use microbes. PILOT combines aspects of an undergraduate research experience with an undergraduate teaching assistantship for an upper‐division lab course focused on molecular biology techniques. Students can leverage these experiences to secure an independent research position that may involve an Honors‐in‐the‐Major (HIM) thesis or participation in the Program for Undergraduate Research Experience (PURE). All of the aforementioned activities provide authentic research experiences while also promoting the development of soft skills essential for success in research. This poster will provide an overview of the CUREs and research programs available to life science students at UCF. Each program can serve as a template for similar efforts at other Universities.Support or Funding InformationNational Science Foundation S‐STEM grant 1742380This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Are You a Scientist? Exploring Science Identity in a Structural Biology Outreach Program
Authors: Wyatt Brittney Nicole , Schram Malia 
Published: June 2021

As part of the science community, scientists are agents of social influence that can impact a student's sense of belonging and participation in science. Students mentored in research experiences have an increase in science persistence, efficacy, and identity. To further investigate the effect of mentored research experiences on a student's science identity, we developed a research‐intensive outreach lab dedicated to instructing high school students and undergraduate research mentors on techniques used in structural biology. Lab participants expressed fluorescent proteins in bacteria and purified the proteins to subsequently determine the proteins' structure by X‐ray crystallography. The development of this outreach lab raised specific questions on the effectiveness of engaging students in science through outreach programs. Specifically, does an inquiry‐based science outreach program increase students' perception of themselves as a scientist by doing hands on experiments, group discussions and pre/post‐lab assignments? Prior to participation in the outreach program, a majority of the students already strongly identified as a science person. While the students' perceptions of themselves as a science person did not change, how students viewed scientists changed from impersonal to personal characteristics after completion of the program. Students indicated that the inclusive environment of the outreach program created an authentic sense of belonging in a research setting. Based on these results, future work will focus on modifying and expanding mentored research programs to engage a range of students in research experiences.Support or Funding InformationThis work was supported by Dr. Martin St. Maurice and the Marquette University Strategic Innovation Fund.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Making Experiential Education in the Lab Accessible: Reflections of Deaf or Hard‐of‐Hearing Students and Lab Advisors
Authors: Gehret Austin U. 
Published: June 2021

The value of an undergraduate research or internship experience can be measured by its ability to transform a student's self‐identity related to science, technology, engineering and mathematics (STEM). Successful experiences not only hold potential to help students shed previously held notions of self‐incompatibility with STEM, they can often motivate a research career and the desire to develop as a scientist. However, students of diverse and underrepresented populations, such as d/Deaf and hard‐of‐hearing students (DHH), engaged in undergraduate research or internship experiences in STEM may or may not reap these same benefits given the potential for barriers to information access. We conducted a survey of current and past DHH undergraduate students who worked in a lab setting as part of an undergraduate research or internship experience; as well as, graduate and undergraduate research advisors and internship advisors. All of the advisors had little to no sign language skills and had worked with at least one DHH student. Students and advisors were asked to provide strategies that they used to facilitate training and communication in lab and to rank the perceived effectiveness of those strategies. Students placed a strong emphasis on the benefits of access services (e.g., interpreting, captioning) and sign language while advisors ranked written communication highest with written protocols and face‐to‐face communication on par with access services. When asked to reflect upon these experiences, students and advisors were largely in agreement that the experiences were rewarding and productive, respectively. In contrast, DHH graduate students with prior lab research experiences indicated a readiness for graduate‐level research that graduate advisors disputed.Support or Funding InformationThis work was supported by an internal NTID FEAD grant (A.U.G.)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Developing an Inclusive Workshop Series for Faculty Mentoring Diverse Research Students
Authors: Michel Lea Vacca , Newman Dina , Magalhaes Rita Margarida Almeida , Wyatt Brittney N 
Published: June 2021

Undergraduate research can be an incredibly rewarding experience for both students and mentors. Many students who participate in undergraduate research find themselves motivated to pursue graduate programs in their fields. However, a negative experience during undergraduate research can have the opposite effect‐ students may disengage from scientific research altogether, and mentors may find themselves pulling back from mentoring undergraduates. When students are from nontraditional or underrepresented groups, these effects can be amplified due to complicating factors such as stereotype threat and a deflated sense of belonging. Here, we report on a workshop series for research mentors, designed specifically to improve and enhance faculty awareness on inclusive practices. The workshops employed a combination of reading and writing assignments, discussions, videos, podcasts, and activities to help mentors recognize the complexity of identity, implement inclusive practices in their research groups, and foster a sense of belonging in their students. A majority of faculty who participated in the workshops reported having a positive experience that increased their awareness and promoted them to be a more reflective research mentor.Support or Funding InformationThe development of this workshop series was supported by an Inclusive Excellence grant from the Howard Hughes Medical Institute (PI: Scott Franklin, RIT).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Development of a directed beam monochromatic UV light device for investigation of DNA damage in skin cancer
Authors: Paliwal Vipin , Masoud Nazieh 
Published: June 2021

Skin cancer is one of the most common forms of cancer in US. Prolonged exposure to sunlight is one of the major causes of skin cancer. UV‐B radiations in the region of 290–320 nm of the solar spectrum are absorbed by skin cells resulting in mutated DNA leading to cancer. A need to for a directed beam source of single wavelength UVB light to study DNA damage prompted us to develop this light source. We developed a small portable UVB light source with directed beam emitting single wavelength at 308 nm. A mixture of Xe and Cl was used to form the XeCl* excimer which specifically emits the wavelength of 308 nm. The source is completely sealed and portable and can be transported to any laboratory, classroom or clinic. The source generates UVB light inside a ¼ inch diameter sealed quartz tube such that the light leaves from one end of the tube (directed beam) which can be regulated in intensity. The utility of the UVB source was tested by studying quantitative DNA damage (6–4 photoproducts) in calf thymus DNA. We conclude that the formation of 6–4 pyrimidine‐pyrimidone photoproducts is proportional to the dose of UVB radiation. In addition to skin cancer research, future application of the source could also include classroom demonstrations and even precision laser phototherapy of skin conditions such as Vitiligo.Support or Funding InformationMilwaukee School of Engineering □ Summer Professional Development Grant‐2018This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
DNA Repair Process in Virally Infected Cells
Authors: Podlutskaya Viktorija , Bishop Sabrina , Haines Samanta , Podlutsky Andrej 
Published: June 2021

Humans come into regular contact with a spectrum of infectious agents, such as viruses. According to the CDC, there are over 200 viruses that contribute to just the common cold. Viruses will infect host cell DNA and begin to produce new viruses. In addition to viral challenges, cells must defend against endogenous threats such as oxidative stress, which cause a variety of DNA damage and could lead to mutations. These and other stimuli result in cellular efforts to repair DNA, but sometimes the damage is not repaired properly. This may occur because of viruses hijacking the DNA repair machinery while cells attempt to repair their DNA. Our hypothesis is that the virus‐infected cells could not repair their damaged DNA properly and as a result, damage is passed onto subsequent generations in the form of mutations. Accumulation of damaged and mutated DNA results in a predisposition to cancer and subsequent progression to tumor formation. For example, individuals infected with HIV/AIDS, caused by a virus, show a greater increase in certain types of cancer. Using Human Herpes Virus 8, the show the link between virus infections and cellular DNA repair function. Through measuring DNA repair with the Comet Assay, and by analyzing the level of apoptosis, we conclude that active production HHV8 in BCBL1 cells interfere with the DNA repair of X‐ray and UV‐C induced DNA damage.Support or Funding Information1) Research reported in this publication was supported by the National Institute Of General Medical Sciences of the National Institutes of Health under Award Numbers UL1GM118991, TL4GM118992, or RL5GM118990. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. UA is an AA/EO employer and educational institution and prohibits illegal discrimination against any individual: www.alaska.edu/titleIXcompliance/nondiscrimination.2) NASA EPSCoR, NNH15ZHA003CThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Compromised Genomic Maintenance Integrity after Non‐Lethal Doses of Cadmium
Authors: Sherrer Shanen M. , Lundh Linnea M. 
Published: June 2021

The integrity of an organism's genome can be compromised and promote carcinogenesis without structural modifiers under certain conditions. One such condition occurs when cadmium is present since cadmium exposure is linked to lung cancer and other cancers with little molecular details known. In this study, we first observed that the productivity of replicative DNA polymerases is greatly reduced in the presence of cadmium. This cadmium‐induced decrease in DNA polymerase efficiency can lead to an increase in genetic mutations that become substrates for the DNA mismatch repair (MMR). Deficiency of MMR also increases spontaneous mutability and is the cause of some sporadic cancers and colon cancer. Interestingly, cadmium selectively inhibits 3′‐directed MMR, a reaction that absolutely depends on human MutLα (hMutLα), and that can only be restored with supplementation of endonuclease‐active hMutLα. We also found that cadmium specifically inactivates hMutLα endonuclease activity. Based on our findings, it is suggested that some of the biological effects of cadmium on MMR are the result of deminished replicative DNA polymerase activity, and selective inhibition of zinc‐dependent hMutLα. Thus, our work provides new molecular details on how cadmium acts as an environmental carcinogen and mutagen.Support or Funding InformationThis work was partially financially supported by St. Mary's College of Maryland. L. Lundh was supported by the Cove Point Natural Heritage Trust's Ruth Mathes Scholarship.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Elongin and the Elongin A ubiquitin ligase complex in transcription and the response to DNA damage
Authors: Weems Juston Cory , Conaway Joan , Conaway Ron 
Published: June 2021

Lesions induced by a variety of DNA damaging agents can block RNA polymerase II (Pol II) elongation. Mechanisms that reactivate or remove Pol II that has become stalled or arrested at such lesions are critical for resumption of gene expression after DNA damage repair and, in addition, may contribute to efficiency of the DNA repair process by enhancing access of the damage repair machinery to the lesion. Following exposure of cells to UV irradiation or other DNA damaging agents, Pol II is ubiquitinated in a transcription‐coupled reaction and degraded by the proteasome, and it has been proposed that ubiquitination and degradation of Pol II stalled at DNA lesions may contribute to transcription‐coupled DNA repair and/or to reactivation of transcription after repair of the damaged DNA.Elongin is a multisubunit complex that was first identified and purified as an activity that stimulates the rate at which Pol II elongates nascent transcripts in vitro. Elongin is composed of 3 subunits, Elongin A (ELOA), the ubiquitin‐like protein Elongin B (ELOB), and Elongin C (ELOC), which is similar to the SCF ubiquitin ligase subunit Skp1. Elongin A performs dual functions in cells as a component of RNA polymerase II (Pol II) transcription elongation factor Elongin and as the substrate recognition subunit of a Cullin‐RING (CRL) E3 ubiquitin ligase that has been shown to target Pol II stalled at sites of DNA damage. Here we investigate the mechanism(s) governing conversion of the Elongin complex from its elongation factor to its ubiquitin ligase form. We find that assembly of the Elongin A ubiquitin ligase is a tightly regulated process. In unstressed cells, the majority of Elongin A is found as part of Pol II elongation factor Elongin. Assembly of Elongin A into the ubiquitin ligase is strongly induced by genotoxic stress, by transcriptional stresses that lead to accumulation of stalled Pol II, and by other stimuli, including endoplasmic reticulum and nutrient stress and retinoic acid signaling, that activate Elongin A‐dependent transcription. We will describe ongoing studies to define signal transduction pathways that lead to assembly and activation of the Elongin A‐ubiquitin ligase as well as experiments addressing the possibility that the Elongin A ubiquitin ligase plays a more direct role in Elongin A‐dependent transcription activation than previously anticipated.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
CoxR Directly Represses Alkane Hydroxylase Gene Expression in Caulobacter crescentus
Authors: Abbondanza Domenic , Kaufman Marissa , Smolarek Brandon , Dey Arup , Peterson Celeste 
Published: June 2021

Alkanes are commonly found in nature and many gram positive and gram negative bacteria have developed enzymes for degrading them. The alphaproteobacteria Caulobacter crescentus has the CYP153 gene which codes for a medium‐chain alkane hydroxylase in the cytochrome P450 family. However, the regulatory mechanism controlling this gene has not been well‐characterized. A reverse genetics screen found that a deletion in the TetR family coxR gene results in a strain that is sensitive to oxidative stress. We used RNA‐seq and EMSA with Ni‐NTA purified CoxR to determine which genes CoxR directly regulates. Expression of the CYP153, ferredoxin and ferredoxin reductase genes were shown to be upregulated in the coxR deletion strain. Furthermore, CoxR was shown to directly bind to a 35bp region of the CYP153 promoter. In summary, we have shown that the transcription factor CoxR directly represses CYP153 gene expression.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Role of CREG1 as a Master Regular of Liver Function
Authors: Jahan Iffat , Bulla Gary A 
Published: June 2021

Mammalian development involves a complex system of regulatory signals and reactions resulting in highly differentiated cell types with specific structure and function. The liver is a major organ that has been studied extensively to understand underlying genetic processes responsible for specification, establishment and maintenance of tissue identity. Hepatoma and hepatoma variant cell lines have been used as a model to understand genetic networks responsible for liver function. Whole genome microarray analysis of hepatocyte cell lines has revealed candidate genes that may serve as regulators or master regulators of liver specificity. In two previous studies, the role of candidate gene Cellular Repressor of E1A Stimulated Gene (CREG1) on regulation of liver‐specific gene expression was determined using transfection studies combined with utilization of quantitative real‐time polymerase chain reaction (qRTPCR). Both studies found strong activation (10–100‐fold) of transcription factor Hnf6 and the downstream gene Serpina1 (a marker gene used to identify liver function). These findings suggested that CREG1 might act through Hnf6 to regulate Serpina1 via a Locus Control Region (LCR). However, while one study showed that of CREG1 overexpression in a hepatoma variant cell line resulted in modest activation of liver‐specific transcription factors Hnf1, Hnf4 and Hnf3, the second study suggested robust activation of these genes as measured by qRT‐PCR. In the current study, a CREG1 expression vector was reintroduced into two variant cell lines and gene activation profiles monitored to establish validity of the previous studies. However, we postulated that CREG‐1 overexpression, validated by qRT‐PCR, can activate expression of hepatocyte transcription factor Hnf6 and the downstream gene Serpina1.However, analysis of gene silencing of liver and non‐liver cell types using whole genome microarray screening will help to identify, compare and elucidate the effects of various candidate tissue specific genes. Moreover, we are currently interested to see the reintroduction of liver‐enriched factors in hepatoma variants fully reactivates liver gene expression. Thus, understanding the underlying mechanism and role of each gene helps to develop therapeutic treatment targets for treating liver diseases.Support or Funding InformationEastern Illinois University, Department of Biological ScienceThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Kub5‐HeraRPRD1B regulates CDK1 expression through the DREAM complex
Authors: YEH I‐JU , Motea Edward A , Boothman David A 
Published: June 2021

Triple Negative Breast Cancer (TNBC) is a subtype with more aggressive, less differentiated capacity and enhanced metastatic ability. Although TNBC tumors are more responsive to neoadjuvant chemotherapy compared to receptor‐positive tumors, development of resistance to cytotoxic chemotherapy and early relapse is more common. Due to the lack of effective therapies, understanding the underlying mechanisms of TNBC aggressiveness and poor prognosis is a major focus of research with particular interest in identifying new therapeutic targets.Kub5‐HeraRPRD1B (K‐H) is a novel factor involved in preserving genomic stability and regulates BRCA1 function by mediating the expression of CDK1, a master regulator of cell cycle, DNA replication, and DNA repair. This regulation has been reported in MDA‐MB‐231 cells, a model of TNBC. However, the underlying mechanism regulated CDK1 expression by K‐H is unknown. Here, we found that the CDK1 promoter is essential for the recruitment of K‐H. We also examined the interaction between K‐H and the complex for the regulation of cell cycle‐dependent gene expression, DREAM complex (dimerization partner, RB‐like, E2F and multi‐vulval class B complex) by immunoprecipitation. The interaction between K‐H and the DREAM complex is further validated using a Proximity ligation assay (PLA). Furthermore, a mutation in K‐H (R106A) results in the loss of an interaction between K‐H and the DREAM complex as well as K‐H and RNAPII, leading to decreased CDK1 levels. These results suggest that CDK1 expression is upregulated by K‐H and its complex formation with the DREAM complex and RNAPII. Thus, we hypothesize that K‐H modulates CDK1 expression through the recruitment of the DREAM complex to the CDK1 promoter region in a sequence‐specific manner. Our studies reveal a novel strategy for developing therapies that target the interaction between K‐H and the DREAM complex, potentially inhibiting the growth of cancer cells.Support or Funding InformationThis work is supported by NIH grant 1 R01 CA201489‐04This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.