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Torres, A. A.

Publications and source records attributed to Torres, A. A..

2 recordsLinked to original sources

Ivermectin resistance in dung beetles exposed for multiple generations

Ivermectin is an antiparasitic drug commonly used in cattle, that is excreted in dung, causing lethal and sub-lethal effects on coprophagous non-target fauna. Given that cattle parasites generate resistance to ivermectin, farmers have increased the used doses, with a consequent threat to wild fauna. The dung beetle species Euoniticellus intermedius provides ecosystem services by burying dung in cattle pastures, however it is highly threatened by ivermectin. Here we experimentally tested whether E. intermedius generates resistance against ivermectin after being exposed for several generations to a sublethal dose. We generated two laboratory lines where beetles were exposed to either ivermectin-treated or ivermectin-free dung for 18 generations. We compared reproductive success (total brood balls, emerged beetles, proportion emerged and days to emergence) of beetles from both lines across generations. Additionally, for each line, we carried-out toxicity experiments with increasing ivermectin concentrations to determine if sensitivity to ivermectin was reduced after some generations of exposure (i. e. if beetles acquired ivermectin resistance by means of transgenerational effects). Our results show that dung beetles do not generate resistance to ivermectin after 18 generations of continuous exposure and quantitative genetic analyses show low genetic variation in response to ivermectin across generations. Together, these results indicate low potential for adaptation to the contaminant in the short term. Although we cannot exclude that adaptation could occur in the long term, our results and comparative evidence in other insects indicate that dung beetles, and probably other species, are at risk of extinction in ivermectin-contaminated pastures unless they are pre-adapted to tolerate high ivermectin concentrations.

ecology↗

Spir-1 promotes IRF3 activation and is targetted by vaccinia virus protein K7

Cellular proteins often have multiple and diverse functions. This is illustrated with protein Spir-1 that is an actin nucleator, but, as shown here, also functions to enhance IRF3 activation downstream of RNA sensing by RIG-I/MDA-5. In human and mouse cells lacking Spir-1, IRF3 activation is impaired, whereas Spir-1 overexpression enhanced IRF3 activation. Furthermore in Spir-1-/- cells, the infectious virus titres and sizes of plaques formed by two viruses that are sensed by RIG-I, vaccinia virus (VACV) and Zika virus, are increased. These observations demonstrate the biological importance of Spir-1 in the response to virus infection. Like cellular proteins, viral proteins also have multiple and diverse functions. Here, we also show that VACV virulence factor K7 binds directly to Spir-1 and that a diphenylalanine motif of Spir-1 is needed for this interaction and for Spir-1-mediated enhancement of IRF3 activation. Thus, Spir-1 is a new virus restriction factor and is targeted directly by an immunomodulatory viral protein that enhances virus virulence and diminishes IRF3 activation. Author SummaryInfection of cells by viruses is sensed by host molecules called pattern recognition receptors (PRRs) that activate signalling pathways leading to an anti-viral response. In turn, viruses express proteins that negate these host responses to mediate escape from the anti-viral response. Here, we report that protein K7 from a large DNA virus called vaccinia virus (VACV), binds to a host cell protein called Spir-1. Spir-1 is known to regulate the assembly of actin filaments inside cells, but here we show that Spir-1 also functions to activate the host response to virus infection and to limit the replication and spread of both RNA and DNA viruses. Thus, this study has uncovered new functions of cellular protein Spir-1 as an activator of innate immunity and as a restriction factor for diverse viruses. Further, it shows that Spir-1 is targeted by a virus protein during infection.

microbiology↗