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Susceptibility of amphibians to chytridiomycosis is associated with MHC class II conformation.

Bataille A, Cashins SD, Grogan L, Skerratt LF, Hunter D, McFadden M, Scheele B, Brannelly LA, Macris A, Harlow PS, Bell S, Berger L, Waldman B - Proc. Biol. Sci. (2015)

Bottom Line: We found that Bd-resistant amphibians across four continents share common amino acids in three binding pockets of the MHC-II antigen-binding groove.Rescuing amphibian biodiversity will depend on our understanding of amphibian immune defence mechanisms against Bd.The identification of adaptive genetic markers for Bd resistance represents an important step forward towards that goal.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Behavioral and Population Ecology, School of Biological Sciences, Seoul National University, Seoul 151-747, South Korea.

ABSTRACT
The pathogenic chytrid fungus Batrachochytrium dendrobatidis (Bd) can cause precipitous population declines in its amphibian hosts. Responses of individuals to infection vary greatly with the capacity of their immune system to respond to the pathogen. We used a combination of comparative and experimental approaches to identify major histocompatibility complex class II (MHC-II) alleles encoding molecules that foster the survival of Bd-infected amphibians. We found that Bd-resistant amphibians across four continents share common amino acids in three binding pockets of the MHC-II antigen-binding groove. Moreover, strong signals of selection acting on these specific sites were evident among all species co-existing with the pathogen. In the laboratory, we experimentally inoculated Australian tree frogs with Bd to test how each binding pocket conformation influences disease resistance. Only the conformation of MHC-II pocket 9 of surviving subjects matched those of Bd-resistant species. This MHC-II conformation thus may determine amphibian resistance to Bd, although other MHC-II binding pockets also may contribute to resistance. Rescuing amphibian biodiversity will depend on our understanding of amphibian immune defence mechanisms against Bd. The identification of adaptive genetic markers for Bd resistance represents an important step forward towards that goal.

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Related in: MedlinePlus

Experimental infection of L. v. alpina frogs frompopulations with varied Bd infection histories. (a)Survival curves for captive-reared frogs from two historicallyinfected sites (A and B) and an uninfected site (C) in KosciuszkoNational Park, Australia, experimentally infected with a virulent Bdculture. (b) Mean infection intensity as a functionof time since Bd inoculation for those subjects that survived fiveweeks or less, eight weeks, or through the duration of the 12-weekexperiment. These results include the weekly swabs from up to 30frogs from each site, selected by stratified random sampling basedon days survived. Infection intensity is given in log-transformedZSE. Error bars represent 95% confidence intervals.
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RSPB20143127F2: Experimental infection of L. v. alpina frogs frompopulations with varied Bd infection histories. (a)Survival curves for captive-reared frogs from two historicallyinfected sites (A and B) and an uninfected site (C) in KosciuszkoNational Park, Australia, experimentally infected with a virulent Bdculture. (b) Mean infection intensity as a functionof time since Bd inoculation for those subjects that survived fiveweeks or less, eight weeks, or through the duration of the 12-weekexperiment. These results include the weekly swabs from up to 30frogs from each site, selected by stratified random sampling basedon days survived. Infection intensity is given in log-transformedZSE. Error bars represent 95% confidence intervals.

Mentions: After inoculating frogs with Bd, subjects from long-exposed site A survivedsignificantly longer than those from the other long-exposed site B and naivesite C (Kaplan–Meier p = 0.001; figure 2; electronicsupplementary material, table S6). Many subjects were heavily infected and diedwithin five weeks (figure 2).Infection loads of some individuals from sites A and C stabilized after fiveweeks but increased afterwards, leading to morbidity and mortality after eightweeks. Six of 200 frogs (five from site A, one from site C) demonstrated greatlyreduced loads after three weeks and survived until the end of the experiment(figure 2). Allnon-exposed, control frogs survived until the end of the experiment. Figure 2.


Susceptibility of amphibians to chytridiomycosis is associated with MHC class II conformation.

Bataille A, Cashins SD, Grogan L, Skerratt LF, Hunter D, McFadden M, Scheele B, Brannelly LA, Macris A, Harlow PS, Bell S, Berger L, Waldman B - Proc. Biol. Sci. (2015)

Experimental infection of L. v. alpina frogs frompopulations with varied Bd infection histories. (a)Survival curves for captive-reared frogs from two historicallyinfected sites (A and B) and an uninfected site (C) in KosciuszkoNational Park, Australia, experimentally infected with a virulent Bdculture. (b) Mean infection intensity as a functionof time since Bd inoculation for those subjects that survived fiveweeks or less, eight weeks, or through the duration of the 12-weekexperiment. These results include the weekly swabs from up to 30frogs from each site, selected by stratified random sampling basedon days survived. Infection intensity is given in log-transformedZSE. Error bars represent 95% confidence intervals.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4389617&req=5

RSPB20143127F2: Experimental infection of L. v. alpina frogs frompopulations with varied Bd infection histories. (a)Survival curves for captive-reared frogs from two historicallyinfected sites (A and B) and an uninfected site (C) in KosciuszkoNational Park, Australia, experimentally infected with a virulent Bdculture. (b) Mean infection intensity as a functionof time since Bd inoculation for those subjects that survived fiveweeks or less, eight weeks, or through the duration of the 12-weekexperiment. These results include the weekly swabs from up to 30frogs from each site, selected by stratified random sampling basedon days survived. Infection intensity is given in log-transformedZSE. Error bars represent 95% confidence intervals.
Mentions: After inoculating frogs with Bd, subjects from long-exposed site A survivedsignificantly longer than those from the other long-exposed site B and naivesite C (Kaplan–Meier p = 0.001; figure 2; electronicsupplementary material, table S6). Many subjects were heavily infected and diedwithin five weeks (figure 2).Infection loads of some individuals from sites A and C stabilized after fiveweeks but increased afterwards, leading to morbidity and mortality after eightweeks. Six of 200 frogs (five from site A, one from site C) demonstrated greatlyreduced loads after three weeks and survived until the end of the experiment(figure 2). Allnon-exposed, control frogs survived until the end of the experiment. Figure 2.

Bottom Line: We found that Bd-resistant amphibians across four continents share common amino acids in three binding pockets of the MHC-II antigen-binding groove.Rescuing amphibian biodiversity will depend on our understanding of amphibian immune defence mechanisms against Bd.The identification of adaptive genetic markers for Bd resistance represents an important step forward towards that goal.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Behavioral and Population Ecology, School of Biological Sciences, Seoul National University, Seoul 151-747, South Korea.

ABSTRACT
The pathogenic chytrid fungus Batrachochytrium dendrobatidis (Bd) can cause precipitous population declines in its amphibian hosts. Responses of individuals to infection vary greatly with the capacity of their immune system to respond to the pathogen. We used a combination of comparative and experimental approaches to identify major histocompatibility complex class II (MHC-II) alleles encoding molecules that foster the survival of Bd-infected amphibians. We found that Bd-resistant amphibians across four continents share common amino acids in three binding pockets of the MHC-II antigen-binding groove. Moreover, strong signals of selection acting on these specific sites were evident among all species co-existing with the pathogen. In the laboratory, we experimentally inoculated Australian tree frogs with Bd to test how each binding pocket conformation influences disease resistance. Only the conformation of MHC-II pocket 9 of surviving subjects matched those of Bd-resistant species. This MHC-II conformation thus may determine amphibian resistance to Bd, although other MHC-II binding pockets also may contribute to resistance. Rescuing amphibian biodiversity will depend on our understanding of amphibian immune defence mechanisms against Bd. The identification of adaptive genetic markers for Bd resistance represents an important step forward towards that goal.

Show MeSH
Related in: MedlinePlus