- Title Information
- Title
- Disruption of yfjD Gene in Francisella tularensis
- Type of Resource
- text
- Name:
Personal
- Name Part
- Omonira, Japheth
- Role
- Role Term:
Text
- creator
- Name:
Personal
- Name Part
- Coulombe, Kareen
- Role
- Role Term:
Text
- Reader
- Name:
Personal
- Name Part
- Belenky, Peter
- Role
- Role Term:
Text
- Reader
- Name:
Personal
- Name Part
- Nau, Gerard
- Role
- Role Term:
Text
- Advisor
- Name:
Corporate
- Name Part
- Brown University. Biology and Medicine: Biomedical Engineering
- Role
- Role Term:
Text
- sponsor
- Origin Information
- Copyright Date
- 2018
- Physical Description
- Extent
- vi, 38 p.
- digitalOrigin
- born digital
- Note:
thesis
- Thesis (Sc. M.)--Brown University, 2018
- Genre (aat)
- theses
- Abstract
- Abstract of Disruption of yfjD Gene in Francisella, by Japheth Omonira, ScM., Brown University, May 2018.
Francisella tularensis is the causative agent of tularemia, a zoonotic disease that affects animals and humans. F. tularensis has the ability to infect and replicate in host cells, including macrophages. Infected macrophages produce less cytokines and chemokines, proteins that trigger the pro-inflammatory. F. tularensis’ inhibitory ability allows it to avoid the immune response. Previously, a ΔybeX mutant was shown to stimulate more cytokine production and attenuate bacterial growth and virulence. The ybeX gene is one of three in LVS that encodes for proteins containing CBS pair domains, the other two being FTL_0951 (yfjD), and FTL_1075. In this study, disruption of the yfjD gene was shown to elicit a stronger immune response of mouse macrophages to infection than wildtype. The disruption mutant also inhibits the ability of F. tularensis to secrete protein, a phenotype opposite to that of the ybeX deletion mutant. Proper genetic complementation was not achieved. The phenotypic differences, therefore, have not been definitively proven to be caused by the disruption and not other unexpected changes to the bacteria. However, the yfjD gene is at the end of a reading frame, meaning disruption is unlikely to cause downstream effects. Also, sequencing and immunoblotting show the complementing construct to not be as created and functioning as designed. A functioning complement would suggest the phenotype change to be due to something other than gene disruption. Because the complement construct was not constructed as planned, the varying phenotypes may still be due to gene disruption. Because of these aspects, it is likely, though not certain, that the results seen are caused by gene disruption and not due to other alterations.
- Subject (fast)
(authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/00940117")
- Topic
- Genetics
- Subject (fast)
(authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/00968006")
- Topic
- Immunology
- Subject (fast)
(authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/00967867")
- Topic
- Immune response
- Language
- Language Term (ISO639-2B)
- English
- Record Information
- Record Content Source (marcorg)
- RPB
- Record Creation Date
(encoding="iso8601")
- 20180618
- Identifier:
DOI
- 10.26300/676n-qj03
- Access Condition:
rights statement
(href="http://rightsstatements.org/vocab/InC/1.0/")
- In Copyright
- Access Condition:
restriction on access
- Collection is open for research.