Identifying Targets of Small Regulatory RNAs: Transcriptomics in the Carcinogenic Pathogen, Helicobacter pylori
Faculty Mentor
Andrea Castillo, PhD
Presentation Type
Oral Presentation
Start Date
5-7-2024 12:00 PM
End Date
5-7-2024 12:20 PM
Location
PAT 328
Primary Discipline of Presentation
Biology
Abstract
The carcinogenic bacterial pathogen Helicobacter pylori infects half of humankind, leaving the infected at risk of symptomatic diseases like ulcers and gastritis (10-15%) or cancers like gastric adenocarcinoma (1-2%). Infection of the inhospitable stomach using virulence factors that worsen disease may be regulated in part by H. pylori’s many small RNAs (sRNAs). These short, noncoding RNA molecules bind other RNAs, resulting in increased or decreased gene expression. Because few of H. pylori’s >900 small RNAs are studied, including only one transcribed from a disease/cancer-worsening nonessential chromosomal region (pathogenicity island), we aim to identify target(s) of two sRNAs from the cag pathogenicity island (cagPAI). We developed two mutant strains of H. pylori, each overexpressing (excessively producing) one of two cagPAI sRNAs. To identify which RNA molecule(s) these sRNAs may target, we examine shifts in the H. pylori total transcriptome (all RNA molecules) using next-generation RNA sequencing, supplemented with quantification of changes in putative target abundance using reverse transcription quantitative polymerase chain reaction (RT-qPCR). When compared to the unmodified parent strain’s transcriptome, an sRNA-overexpression mutant strain demonstrating significantly increased/decreased frequency of a given RNA suggests the affected molecule was targeted for regulation by the overexpressed sRNA. Thus, through transcriptomic analysis of these overexpression mutant strains, we hope to identify RNA molecule(s) targeted by two sRNAs from the disease/cancer-worsening cagPAI chromosomal region, informing our understanding of how this bacterium regulates the genetics that make it a formidable carcinogenic pathogen.
Recommended Citation
McPeck, Roxanne N.; Morgan, Olivia F.; and Castillo, Andrea R. PhD, "Identifying Targets of Small Regulatory RNAs: Transcriptomics in the Carcinogenic Pathogen, Helicobacter pylori" (2024). 2024 Symposium. 8.
https://dc.ewu.edu/srcw_2024/op_2024/o4_2024/8
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
Identifying Targets of Small Regulatory RNAs: Transcriptomics in the Carcinogenic Pathogen, Helicobacter pylori
PAT 328
The carcinogenic bacterial pathogen Helicobacter pylori infects half of humankind, leaving the infected at risk of symptomatic diseases like ulcers and gastritis (10-15%) or cancers like gastric adenocarcinoma (1-2%). Infection of the inhospitable stomach using virulence factors that worsen disease may be regulated in part by H. pylori’s many small RNAs (sRNAs). These short, noncoding RNA molecules bind other RNAs, resulting in increased or decreased gene expression. Because few of H. pylori’s >900 small RNAs are studied, including only one transcribed from a disease/cancer-worsening nonessential chromosomal region (pathogenicity island), we aim to identify target(s) of two sRNAs from the cag pathogenicity island (cagPAI). We developed two mutant strains of H. pylori, each overexpressing (excessively producing) one of two cagPAI sRNAs. To identify which RNA molecule(s) these sRNAs may target, we examine shifts in the H. pylori total transcriptome (all RNA molecules) using next-generation RNA sequencing, supplemented with quantification of changes in putative target abundance using reverse transcription quantitative polymerase chain reaction (RT-qPCR). When compared to the unmodified parent strain’s transcriptome, an sRNA-overexpression mutant strain demonstrating significantly increased/decreased frequency of a given RNA suggests the affected molecule was targeted for regulation by the overexpressed sRNA. Thus, through transcriptomic analysis of these overexpression mutant strains, we hope to identify RNA molecule(s) targeted by two sRNAs from the disease/cancer-worsening cagPAI chromosomal region, informing our understanding of how this bacterium regulates the genetics that make it a formidable carcinogenic pathogen.
