Arthropod transcriptional activator protein-1 (AP-1) aids tick-rickettsial pathogen survival in the cold

Autor:	Vikas Taank, John F. Anderson, Hameeda Sultana, Girish Neelakanta, Supreet Khanal
Jazyk:	angličtina
Rok vydání:	2018
Předmět:	0301 basic medicine Genome Insect lcsh:Medicine Tick Models Biological Article Microbiology 03 medical and health sciences Mice Open Reading Frames Gene expression parasitic diseases Gene silencing Animals Amino Acid Sequence RNA Messenger Promoter Regions Genetic lcsh:Science Gene Pathogen Base Pairing Phylogeny Regulation of gene expression Multidisciplinary biology Base Sequence Ixodes lcsh:R biology.organism_classification bacterial infections and mycoses Anaplasma phagocytophilum Adaptation Physiological Cold Temperature Transcription Factor AP-1 030104 developmental biology Gene Expression Regulation Ixodes scapularis Larva Female RNA Interference lcsh:Q
Zdroj:	Scientific Reports, Vol 8, Iss 1, Pp 1-15 (2018) Scientific Reports
ISSN:	2045-2322
DOI:	10.1038/s41598-018-29654-6
Popis:	Ixodes scapularis ticks transmit several pathogens to humans including rickettsial bacterium, Anaplasma phagocytophilum. Here, we report that A. phagocytophilum uses tick transcriptional activator protein-1 (AP-1) as a molecular switch in the regulation of arthropod antifreeze gene, iafgp. RNAi-mediated silencing of ap-1 expression significantly affected iafgp gene expression and A. phagocytophilum burden in ticks upon acquisition from the murine host. Gel shift assays provide evidence that both the bacterium and AP-1 influences iafgp promoter and expression. The luciferase assays revealed that a region of approximately 700 bp upstream of the antifreeze gene is sufficient for AP-1 binding to promote iafgp gene expression. Furthermore, survival assays revealed that AP-1-deficient ticks were more susceptible to cold in comparison to the mock controls. In addition, this study also indicates arthropod AP-1 as a global regulator for some of the tick genes critical for A. phagocytophilum survival in the vector. In summary, our study defines a novel mode of arthropod signaling for the survival of both rickettsial pathogen and its medically important vector in the cold.
Databáze:	OpenAIRE
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