Tag: Oral Session 4S

Chitin Binding Protein GbpA promotes Proliferation In The Drosophila Midgut

Presenter(s): Zoë Wong − Biology, Psychology

Faculty Mentor(s): Karen Guillemin

Oral Session 4S

Research Area: Natural Science (Biology)

The microbes that live both in and on us, collectively known as our microbiota, are estimated to include 3.8 ·1013 cells (Sender, et al., 2016). While this considerable community plays an active role in host health, it also contributes to disease phenotypes including states of inflammation and excess cell proliferation. Previous work has shown that secretion of a bacterial chitin binding protein (CBP), GbpA, by Aeromonas veronii is sufficient to induce cell proliferation in zebrafish (Banse et al., unpublished). Chitin serves as an important Carbon and Nitrogen source for hosts and microbes that can breakdown colloidal chitin (Tran et al., 2011). Interestingly, CBPs are found in microbes that are not capable of utilizing chitin as a nutrient source, which suggests that bacteria have an ulterior motive for CBP translation (Tran et al., 2011). To investigate the relevance of GbpA expression, we propose to use Drosophila melanogaster as a model organism because of their short generation time, ability to be reared germ-free, and established assay for measuring cell proliferation in the midgut epithelium (Jones et al., 2017). We hypothesize that the CBP domain of GbpA (domain 1, GbpAD1) is necessary and sufficient for increased cell proliferation in Drosophila. Chitinases and other CBPs are linked to pro-proliferative states of inflammation and we would expect this result to be replicated in Drosophila (Tran et al., 2011). The highly-conserved sequence identity of CBPs makes it an interesting avenue for exploring the intricacies of bacterial-host interactions.

Effects of Environment and Relatedness on the Gut Microbiome of Ugandan Red Colobus Monkeys

Presenter(s): Tabor Whitney − Biology

Faculty Mentor(s): Nelson Ting

Oral Session 4S

Research Area: Biological Anthropology

Funding: Peter O’Day Fellowship

The gut microbiome consists of microbial communities that reside in the gastro-intestinal tract of living organisms. Variation in this system has been linked to health outcomes in human and animal models by affecting digestion, immune system development, and pathogen invasion. However, we still lack a complete understanding of the factors that shape gut microbiome variation, particularly in wild primates. The central aim of this research is to further test how forest fragmentation is associated with gut microbial diversity in the Ugandan red colobus monkey. We sequenced the 16S rRNA hypervariable V-4 region to characterize the gut microbiome from 106 genotyped individuals across eight social groups inhabiting different forest types within Kibale National Park and its surrounding area. We compared alpha diversity in the gut microbiome of individuals inhabiting fragmented versus continuous forest and did not find a simple relationship between gut microbial diversity and forest fragmentation. While individuals residing in some fragments had lower gut microbiome alpha diversity, those residing in well-protected fragments retained gut microbial diversity levels comparable to residents of continuous forest. Furthermore, we discovered numerous highly related red colobus monkey dyads between forests, which allowed us to assess the affects of genetic relatedness on gut microbial similarity. We found that environment plays a larger role than genetic relatedness in shaping the gut microbiome. Our research thus reinforces the role that environment plays in shaping within-species gut microbial variation with potential implications for the conservation of threatened populations in fragmented landscapes.

Characterization of Lrig1 Positive Stem Cells During Colitis Recovery

Presenter(s): Nicholas Jahahn − General Science

Faculty Mentor(s): Annie Zemper

Oral Session 4S

Research Area: Natural/Physical Science

Funding: National Institute of Diabetes and Digestive and Kidney Diseases, OURS program at the university of Oregon through NIH award

The intestine is a highly regenerative organ in humans and mice. Within the epithelium, structures called crypts contain epithelial stem cells that repopulate the intestinal mucosa. Lrig1 is an ErbB negative regulator that marks a population of stem cells in the base of the intestinal crypts. To study intestinal epithelium in a disease state, Dextran sodium sulfate (DSS) was used to induce ulcerative colitis in mice, characterized by inflammation of the distal colon epithelia. Here we examined the role of Lrig1 positive stem cells in colitis recovery. To accomplish this, we utilized transgenic mice that expressed Cre recombinase protein from the Lrig1 promoter and expressed YFP protein from the ROSA locus. Lineage tracing was carried out to observe what stem cells give rise to when the mouse is treated with DSS. Immunofluorescent analysis was conducted to visualize the localization of Lrig1 positive stem cells and their progeny in the wound healing process for comparison between homeostasis and different durations of recovery. It was observed that at both 36 and 48 hours after a weeklong assault of DSS there was a greater percentage of lineage traced cells found higher in the crypt compared to homeostatic conditions. We further observed that proliferation of the lineage traced cells followed the same trend. These results indicate that Lrig1 stem cells do actively participate in the recovery process. Where exactly the Lrig1 stem cells that participate in recovery originate from will be addressed with further lineage tracing closer to the time of cessation of DSS.

Inflammatory Phenotypes Of Zebrafish Enteric Nervous System Mutants

Presenter(s): Lillian Carroll − Biology

Faculty Mentor(s): Judith Eisen, Kristi Hamilton

Oral Session 4S

Research Area: Natural Science

Funding: OURS Program

Intestinal health depends on the microbial community within the dynamic intestinal environment. The enteric nervous system (ENS) innervates the intestine and modulates the microbial community composition. ENS reduction causes Hirschsprung disease (HSCR), resulting in intestinal dysmotility. Many HSCR patients develop potentially life-threatening intestinal inflammation. HSCR is genetically complex, with multiple HSCR genetic loci. The zebrafish is an excellent model in which to study the relationship between inflammation and genes linked to HSCR. Zebrafish with a mutation in the HSCR gene, sox10, have fewer enteric neurons, increased intestinal epithelial cell proliferation, and develop microbiota-dependent intestinal inflammation. Zebrafish with a mutation in another HSCR gene, ret, also have fewer ENS neurons but do not exhibit increased intestinal inflammation. sox10 acts in neural crest cells that form the ENS and ret acts within ENS cells, thus, I hypothesized that the intestinal phenotype of sox10;ret double mutants would be similar to the phenotype of sox10 mutants. To test this hypothesis, I analyzed the phenotypes of double mutants. I used PCR to identify mutants and quantified inflammation by counting intestinal neutrophils and recently-proliferated intestinal epithelial cells, and by determining the intestinal bacterial abundance. Surprisingly, and contrary to my hypothesis, sox10;ret double mutants did not exhibit increased intestinal inflammation or cell proliferation compared to wild-types. These results prompt me to reconsider the potential interactions

of the mutated genes, which will provide insights into the role of the ENS as a crucial regulator of the intestinal microbial community and its function in the maintenance of intestinal health.

Assessing The Role Of Crossing Structures In Primate Conservation

Presenter(s): India Brock − Biological Anthropology, Environmental Science

Faculty Mentor(s): Frances White, Larry Ulibarri

Oral Session 4S

Research Area: Primate Conservation

Funding: CAS Continuing Student Scholarship

Anthropogenic modification of natural landscapes is an increasing problem for wildlife, including primates. Infrastructure, including roads, have direct and indirect impacts on wildlife and landscapes. Specifically, mortality from collisions with vehicles and dissection of habitats may reduce population sizes, reduce genetic diversity, and increase genetic differentiation. Road ecology is concerned with understanding and mitigating the effects of roads on wildlife. While this research has focused on a number of taxa, research on primates is particularly scarce. Here, we review the literature for studies on crossing structures as a conservation strategy in wild primate populations. We identified 10 publications on this subject that focused on lemurs (N=1), New World monkeys (N=5), Old World monkeys (N=3), and apes (N=1). We also include data on two unpublished studies. Four bridge designs were used in these studies that varied in their dimensions, construction material, and usage across taxonomic categories. We highlight differences in monitoring and usage across each of these studies. This review highlights a paucity of literature on this oft recommended conservation strategy and an inability to collectively build on previous work from lack of publication. We contend that long-term monitoring of crossing structures be integral to studies on crossing structure. A conceptual framework is proposed for the standardization of crossing structure studies include components for designing purpose-built crossing structures, and avenues for appropriately evaluating bridge effectiveness. We urge the scientific and primatologic communities that primate crossing structure use and effectiveness must be scientifically based.