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A genetic life cycle switch in Bacillus thuringiensis virus GIL01

Characteristics of the GIL01 bacteriophage. (A) Schematic view of the surface and the interior of the GIL01 bacteriophage.

Publish Date: 03.12.2018

Category: Outstanding research achievements, Interdisciplinary research, Our contribution to sustainable development goals

Sustainable development goals: 3 Good health and well-being (Indicators)

Bacterial viruses influence the development of bacteria and the transmission of antibiotic resistance genes among bacteria. The elucidation of this mechanisms may provide new weapons to combat antibiotic resistance development in bacteria.

 Authors: Nadine Fornelos, Douglas F. Browning, Anja Pavlin, Zdravko Podlesek, Vesna Hodnik, Margarita Salas, Matej Butala

Viruses that infect bacteria (bacteriophages) represent the most abundant biological entities on the planet, having an enormous impact on microbial communities and bacterial evolution. The studied bacteriophage GIL01 of Bacillus thuringiensis is classified as Tectivirus, members of which are supposed to be the ancestors of many eukaryotic viruses, including certain viruses that endanger human health. An important fundamental scientific discovery of a research, conducted by the researchers of the Biotechnical Faculty in Ljubljana and foreign colleagues (Nadine Fornelos, Douglas F. Browning, Anja Pavlin, Zdravko Podlesek, Vesna Hodnik, Margarita Salas, Matej Butala (lead author)) has elucidated an unknown genetic switch by which the bacterial virus GIL01 triggers a transition from a dormant cycle to the synthesis of new viral particles and their release by lysis of the bacterial cell.

 The process is regulated by two small bacteriophage proteins, which in addition to affecting the host bacteria response to genotoxic stress, enable the virus to change its lifestyle and leaves the host. This research contributes to the understanding of the life cycles of bacteriophages. Although these life cycles are the basis for understanding molecular mechanisms in bacteria they are studied in detail only for a handful of bacteriophages.

 In addition to opportunistic pathogens Bacillus thuringiensis, B. cereus, B. anthracis, tectiviruses also infect bacteria in the genus Streptococcus and Clostridium. The results of the study imply that the above described mechanism is preserved in a number of tectiviruses. Here resolved GIL01 molecular mechanisms enables to set forth research to develop novel antibacterial compounds based on GIL01 small proteins.

 Reference: Fornelos N., Browning D. F., Pavlin A., Podlesek Z., Hodnik V., Salas M., Butala M. Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue, Nucleic Acids Res., 18 (2018), 9432–9443.

Značilnosti bakteriofaga GIL01Značilnosti bakteriofaga GIL01 DNA

Characteristics of the GIL01 bacteriophage. (A) Schematic view of the surface and the interior of the GIL01 bacteriophage. (B) Structure of the bacterial transcription repressor LexA (blue) bound to DNA, aligned with the structure of the gp6 small protein of the GIL01 bacteriophage (red). Both gp6 and LexA control the GIL01 lytic promoter. Protein gp6 is related to the LexA repressor and functions as ae genetic switch that triggers the construction and release of new virus particles which are released from bacteria upon cell lyses. This is the first description of two LexA family member regulators, but with opposinh functions, that control the bacteriophage life cycle switch. 

 Image source: King A. M. Q., Adams M. J., Carstens E. B., Lefkowitz E. J. (Eds.) Virus Taxonomy: Ninth Report of the International Committee on Taxonomy of Viruses, 317-321, Elsevier (2012); Fornelos N., Browning D. F., Pavlin A., Podlesek Z., Hodnik V., Salas M., Butala M. Lytic gene expression in the temperate bacteriophage GIL01 is activated by a phage-encoded LexA homologue, Nucleic Acids Res., 18 (2018), 9432–9443.

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