Affiliations: | |
Project Leader: | Lorna Min min385@tamu.edu Biochemistry |
Faculty Mentor: | Ryland Young, Ph.D. |
Meeting Times:
|
Summer 2016 (complete) |
Team Size:
|
3 (Team Full) |
Open Spots: | 0 |
Special Opportunities:
|
In addition to exploring the exciting field of bacteriophage and gaining Aggie Research Scholar credentials, students who successfully complete the summer term will be eligible to become part of the Center for Phage Technology in the following Fall and Spring semesters. Program may be completed for credit, if so enrolled. |
Team Needs:
|
In order to be part of this team, you must complete Biosafety Level 2 training and be compliant with all safety guidelines. For the summer, a minimum of 12 hours/week is expected from all students. Basic understanding of microbiology technique is preferred but not required. |
Description:
|
Antibiotic overprescription and misuse have contributed to the creation of “superbugs” resistant to, and sometimes even capable of metabolizing, all known antibiotics. As such, the search for novel antibiotics and their targets is becoming increasingly important. Studying “protein antibiotics” produced by small lytic bacteriophages, viruses that infect bacteria, may aid in this effort. Most pharmaceutical antibiotics currently used target the cell wall, a uniquely bacterial cell component vital to structural integrity. Upon impairment of the cell wall, cells swell up and ultimately explode from their high internal pressure. Protein antibiotics have been found to impair the cell wall using similar mechanisms as pharmaceutical antibiotics. E and A2, the protein antibiotics of prototypical small phages fX174 (Microviridae) and Qb (Alloleviviridae), inhibit the cell wall biosynthesis enzymes MurA and MraY respectively. L, the protein antibiotic of prototypical small phage MS2 (Leviviridae), kills bacteria through an unknown mechanism and is currently thought to activate the host autolytic system, causing the host to degrade its own protective cell wall. Additionally, our lab recently discovered that the protein antibiotic M Lys of Leviviridae phage M inhibits the cell wall biosynthesis lipid II flippase MurJ, establishing a new class of antibiotics that targets flippases specifically. The discovery of protein antibiotics, then, is key to further development of pharmaceutical antibiotics. As such, isolating the phages encoding these protein antibiotics is also becoming increasingly important. This project will therefore focus on the isolation and characterization of novel small lytic phages. |