Determining how two small RNA molecules regulate infection-associated genes in Helicobacter pylori
Faculty Mentor
Andrea Castillo
Presentation Type
Poster
Start Date
4-14-2026 11:30 AM
End Date
4-14-2026 1:30 PM
Location
PUB NCR
Primary Discipline of Presentation
Biology
Abstract
Helicobacter pylori is a bacterial pathogen associated with most cases of duodenal ulcers, MALT lymphoma, and gastric cancer. Approximately 50% of the human population harbors H. pylori in their stomachs—a harsh, constantly changing environment—and 10-20% of those infected develop disease. To navigate environmental challenges and facilitate host infection, H. pylori tightly regulates its gene expression. Infection by H. pylori expressing the CagA protein is fundamental to the host’s development of cancer. CagA is injected into host cells by a syringe-like protein structure called a type 4 secretion system (T4SS). The regulation of genes expressed during this harmful process is understudied. Data suggest that over 60 small RNAs (sRNAs) in H. pylori may partially orchestrate its gene expression. sRNAs typically modulate gene expression by binding to mRNA molecules, repressing their translation and leading to degradation of the target mRNA. Previous work in the Castillo lab identified four mRNA targets—cagβ, cagα, cagZ, and cagY—encoding proteins of the T4SS to be regulated by sRNAs HPnc2540 and HPnc2620, but their mechanism of regulation remains unknown. I have confirmed downregulation of this set of mRNA targets by RT-qPCR and identified potential sRNA-mRNA binding sites using IntaRNA 2.0, a software that has accurately predicted sRNA binding sites in bacterial studies. I aim to experimentally verify predicted interactions of HPnc2540 and HPnc2620 to the cagY mRNA; CagY is fundamental to CagA translocation and is encoded by the first gene of a putative operon also containing cagβ, cagα, and cagZ. This work will determine regulatory networks essential to H. pylori infection.
Recommended Citation
George, Marion, "Determining how two small RNA molecules regulate infection-associated genes in Helicobacter pylori" (2026). 2026 Symposium. 23.
https://dc.ewu.edu/srcw_2026/ps_2026/p2_2026/23
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
Determining how two small RNA molecules regulate infection-associated genes in Helicobacter pylori
PUB NCR
Helicobacter pylori is a bacterial pathogen associated with most cases of duodenal ulcers, MALT lymphoma, and gastric cancer. Approximately 50% of the human population harbors H. pylori in their stomachs—a harsh, constantly changing environment—and 10-20% of those infected develop disease. To navigate environmental challenges and facilitate host infection, H. pylori tightly regulates its gene expression. Infection by H. pylori expressing the CagA protein is fundamental to the host’s development of cancer. CagA is injected into host cells by a syringe-like protein structure called a type 4 secretion system (T4SS). The regulation of genes expressed during this harmful process is understudied. Data suggest that over 60 small RNAs (sRNAs) in H. pylori may partially orchestrate its gene expression. sRNAs typically modulate gene expression by binding to mRNA molecules, repressing their translation and leading to degradation of the target mRNA. Previous work in the Castillo lab identified four mRNA targets—cagβ, cagα, cagZ, and cagY—encoding proteins of the T4SS to be regulated by sRNAs HPnc2540 and HPnc2620, but their mechanism of regulation remains unknown. I have confirmed downregulation of this set of mRNA targets by RT-qPCR and identified potential sRNA-mRNA binding sites using IntaRNA 2.0, a software that has accurately predicted sRNA binding sites in bacterial studies. I aim to experimentally verify predicted interactions of HPnc2540 and HPnc2620 to the cagY mRNA; CagY is fundamental to CagA translocation and is encoded by the first gene of a putative operon also containing cagβ, cagα, and cagZ. This work will determine regulatory networks essential to H. pylori infection.
