TY  - JOUR
A1  - Esmaeilishirazifard, Elham
A1  - Usher, Louise
A1  - Trim, Carol
A1  - Denise, Hubert
A1  - Sangal, Vartul
A1  - Tyson, Gregory H.
A1  - Barlow, Axel
A1  - Redway, Keith F.
A1  - Taylor, John D.
A1  - Kremyda-Vlachou, Myrto
A1  - Davies, Sam
A1  - Loftus, Teresa D.
A1  - Lock, Mikaella M. G.
A1  - Wright, Kstir
A1  - Dalby, Andrew
A1  - Snyder, Lori A. S.
A1  - Wuster, Wolfgang
A1  - Trim, Steve
A1  - Moschos, Sterghios A.
T1  - Bacterial adaptation to venom in snakes and arachnida
JF  - Microbiology spectrum
N2  - Notwithstanding their 3 to 5% mortality, the 2.7 million envenomation-related injuries occurring annually-predominantly across Africa, Asia, and Latin America-are also major causes of morbidity. Venom toxin-damaged tissue will develop infections in some 75% of envenomation victims, with E. faecalis being a common culprit of disease; however, such infections are generally considered to be independent of envenomation. 
Animal venoms are considered sterile sources of antimicrobial compounds with strong membrane-disrupting activity against multidrug-resistant bacteria. 
However, venomous bite wound infections are common in developing nations. Investigating the envenomation organ and venom microbiota of five snake and two spider species, we observed venom community structures that depend on the host venomous animal species and evidenced recovery of viable microorganisms from black-necked spitting cobra (Naja nigricollis) and Indian ornamental tarantula (Poecilotheria regalis) venoms. Among the bacterial isolates recovered from N. nigricollis, we identified two venom-resistant, novel sequence types of Enterococcus faecalis whose genomes feature 16 virulence genes, indicating infectious potential, and 45 additional genes, nearly half of which improve bacterial membrane integrity. 
Our findings challenge the dogma of venom sterility and indicate an increased primary infection risk in the clinical management of venomous animal bite wounds. IMPORTANCE Notwithstanding their 3 to 5% mortality, the 2.7 million envenomation-related injuries occurring annually-predominantly across Africa, Asia, and Latin America-are also major causes of morbidity. Venom toxin-damaged tissue will develop infections in some 75% of envenomation victims, with E. faecalis being a common culprit of disease; however, such infections are generally considered to be independent of envenomation. Here, we provide evidence on venom microbiota across snakes and arachnida and report on the convergent evolution mechanisms that can facilitate adaptation to black-necked cobra venom in two independent E. faecalis strains, easily misidentified by biochemical diagnostics. 
Therefore, since inoculation with viable and virulence gene-harboring bacteria can occur during envenomation, acute infection risk management following envenomation is warranted, particularly for immunocompromised and malnourished victims in resource-limited settings. 
These results shed light on how bacteria evolve for survival in one of the most extreme environments on Earth and how venomous bites must be also treated for infections.
KW  - drug resistance evolution
KW  - extremophiles
KW  - genome analysis
KW  - microbiome
KW  - multidrug resistance
KW  - venom
Y1  - 2022
U6  - https://doi.org/10.1128/spectrum.02408-21
SN  - 2165-0497
VL  - 10
IS  - 3
PB  - American Society for Microbiology
CY  - Birmingham, Ala.
ER  - 
TY  - GEN
A1  - Zancolli, Giulia
A1  - Baker, Timothy G.
A1  - Barlow, Axel
A1  - Bradley, Rebecca K.
A1  - Calvete, Juan J.
A1  - Carter, Kimberley C.
A1  - de Jager, Kaylah
A1  - Owens, John Benjamin
A1  - Price, Jenny Forrester
A1  - Sanz, Libia
A1  - Scholes-Higham, Amy
A1  - Shier, Liam
A1  - Wood, Liam
A1  - Wüster, Catharine E.
A1  - Wüster, Wolfgang
T1  - Is hybridization a source of adaptive venom variation in rattlesnakes?
BT  - a test, using a crotalus scutulatus × viridis hybrid zone in southwestern New Mexico
T2  - Toxins
N2  - Venomous snakes often display extensive variation in venom composition both between and within species. However, the mechanisms underlying the distribution of different toxins and venom types among populations and taxa remain insufficiently known. Rattlesnakes (Crotalus, Sistrurus) display extreme inter-and intraspecific variation in venom composition, centered particularly on the presence or absence of presynaptically neurotoxic phospholipases A2 such as Mojave toxin (MTX). Interspecific hybridization has been invoked as a mechanism to explain the distribution of these toxins across rattlesnakes, with the implicit assumption that they are adaptively advantageous. Here, we test the potential of adaptive hybridization as a mechanism for venom evolution by assessing the distribution of genes encoding the acidic and basic subunits of Mojave toxin across a hybrid zone between MTX-positive Crotalus scutulatus and MTX-negative C. viridis in southwestern New Mexico, USA. Analyses of morphology, mitochondrial and single copy-nuclear genes document extensive admixture within a narrow hybrid zone. The genes encoding the two MTX subunits are strictly linked, and found in most hybrids and backcrossed individuals, but not in C. viridis away from the hybrid zone. Presence of the genes is invariably associated with presence of the corresponding toxin in the venom. We conclude that introgression of highly lethal neurotoxins through hybridization is not necessarily favored by natural selection in rattlesnakes, and that even extensive hybridization may not lead to introgression of these genes into another species.
T3  - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 443 
KW  - adaptation
KW  - Crotalus
KW  - evolution
KW  - hybridization
KW  - introgression
KW  - Mojave toxin
KW  - molecular evolution
KW  - venom
Y1  - 2018
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-407595
ER  - 
TY  - JOUR
A1  - Zancolli, Giulia
A1  - Baker, Timothy G.
A1  - Barlow, Axel
A1  - Bradley, Rebecca K.
A1  - Calvete, Juan J.
A1  - Carter, Kimberley C.
A1  - de Jager, Kaylah
A1  - Owens, John Benjamin
A1  - Price, Jenny Forrester
A1  - Sanz, Libia
A1  - Scholes-Higham, Amy
A1  - Shier, Liam
A1  - Wood, Liam
A1  - Wüster, Catharine E.
A1  - Wüster, Wolfgang
T1  - Is Hybridization a Source of Adaptive Venom Variation in Rattlesnakes? A Test, Using a Crotalus scutulatus x viridis Hybrid Zone in Southwestern New Mexico
JF  - Toxins
N2  - Venomous snakes often display extensive variation in venom composition both between and within species. However, the mechanisms underlying the distribution of different toxins and venom types among populations and taxa remain insufficiently known. Rattlesnakes (Crotalus, Sistrurus) display extreme inter-and intraspecific variation in venom composition, centered particularly on the presence or absence of presynaptically neurotoxic phospholipases A2 such as Mojave toxin (MTX). Interspecific hybridization has been invoked as a mechanism to explain the distribution of these toxins across rattlesnakes, with the implicit assumption that they are adaptively advantageous. Here, we test the potential of adaptive hybridization as a mechanism for venom evolution by assessing the distribution of genes encoding the acidic and basic subunits of Mojave toxin across a hybrid zone between MTX-positive Crotalus scutulatus and MTX-negative C. viridis in southwestern New Mexico, USA. Analyses of morphology, mitochondrial and single copy-nuclear genes document extensive admixture within a narrow hybrid zone. The genes encoding the two MTX subunits are strictly linked, and found in most hybrids and backcrossed individuals, but not in C. viridis away from the hybrid zone. Presence of the genes is invariably associated with presence of the corresponding toxin in the venom. We conclude that introgression of highly lethal neurotoxins through hybridization is not necessarily favored by natural selection in rattlesnakes, and that even extensive hybridization may not lead to introgression of these genes into another species.
KW  - adaptation
KW  - Crotalus
KW  - evolution
KW  - hybridization
KW  - introgression
KW  - Mojave toxin
KW  - molecular evolution
KW  - venom
Y1  - 2016
U6  - https://doi.org/10.3390/toxins8060188
SN  - 2072-6651
VL  - 8
PB  - MDPI
CY  - Basel
ER  - 
TY  - JOUR
A1  - Dennis, Alice B.
A1  - Patel, Vilas
A1  - Oliver, Kerry M.
A1  - Vorburger, Christoph
T1  - Parasitoid gene expression changes after adaptation to symbiont-protected hosts
JF  - Evolution
N2  - Reciprocal selection between aphids, their protective endosymbionts, and the parasitoid wasps that prey upon them offers an opportunity to study the basis of their coevolution. We investigated adaptation to symbiont‐conferred defense by rearing the parasitoid wasp Lysiphlebus fabarum on aphids (Aphis fabae) possessing different defensive symbiont strains (Hamiltonella defensa). After ten generations of experimental evolution, wasps showed increased abilities to parasitize aphids possessing the H. defensa strain they evolved with, but not aphids possessing the other strain. We show that the two symbiont strains encode different toxins, potentially creating different targets for counter‐adaptation. Phenotypic and behavioral comparisons suggest that neither life‐history traits nor oviposition behavior differed among evolved parasitoid lineages. In contrast, comparative transcriptomics of adult female wasps identified a suite of differentially expressed genes among lineages, even when reared in a common, symbiont‐free, aphid host. In concurrence with the specificity of each parasitoid lineages’ infectivity, most differentially expressed parasitoid transcripts were also lineage‐specific. These transcripts are enriched with putative venom toxins and contain highly expressed, potentially defensive viral particles. Together, these results suggest that wild populations of L. fabarum employ a complicated offensive arsenal with sufficient genetic variation for wasps to adapt rapidly and specifically to their hosts’ microbial defenses.
KW  - Adaptation
KW  - experimental evolution
KW  - gene expression
KW  - Lysiphlebus fabarum
KW  - parasitoid
KW  - venom
Y1  - 2017
U6  - https://doi.org/10.1111/evo.13333
SN  - 0014-3820
SN  - 1558-5646
VL  - 71
SP  - 2599
EP  - 2617
PB  - Wiley
CY  - Hoboken
ER  -