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Written by | Snow Moon
| Enzymatic
parasites can increase the pressure of host evolutionary selection and promote immune evolution
.
However, sometimes this selection evolution does not always go in the direction
of increasing resistance.
Resistance-based immune responses can have undesirable consequences that affect host survival and reproduction
by consuming limited resources or inducing autoimmune diseases that reduce host fitness.
Evolutionary optimization theory suggests that evolutionary increased parasite resistance must be balanced
against the cost of immune response.
Only in this way can evolution move in the direction of optimal resistance and immune response
.
Populations may evolve to tolerate, allowing infection to persist while reducing infection mortality and reproductive costs
.
Tolerance itself is expensive and either drains energy to repair damage or allows infection
.
Intraspecific variations in immune costs are rarely studied in a pattern-evolved manner, and there are few models
of tolerance or resistance.
Daniel I.
Bolnick's team from the University of Texas at Austin published an article in Science titled Evolutionary gain and loss of a pathological immune response to parasitism
。 Modelled on sticklebackfish in two lakes, the study explored the effects
of balancing gains and damage in tapeworm infection on the evolution of immune tolerance and resistance populations.
The marine population of the three-spined fish Gasterosteus aculeatus encountered freshwater tapeworms less often and therefore did not evolve resistance
.
Later, marine threefish established populations in freshwater, thus evolving resistance
.
But infection rates also vary from lake to lake, and sometimes prevalence varies
even for similar lakes.
The authors noted that the infection rates of sticklebacks in Lake Roberts and Lake Gaolings (R and G) diverged to 0 and greater than 50%, and the two were located in close
proximity.
The authors hypothesize that differences in infection prevalence reflect the evolution of resistance in R sticklebacks and tolerance in G
sticklebacks.
The authors crossed sticklebacks from R and G and exposed them to schizocephalus tapeworm
.
The analysis found that the infection rate of hybrid sticklebackfish with a large proportion of R was low
.
When tapeworms reach 50 mg, birds come to fish, and birds are the end hosts
of tapeworms.
The growth of tapeworms in the backcrossed sticklebacks is inhibited and does not reach this threshold, protecting the fish from predation
.
The contrast found that R sticklebacks produced more ROS in granulocytes after infection and showed severe peritoneal fibrosis
.
In vertebrates, parasites cause tissue damage, leading to inflammation, fibroblast proliferation, collagen deposition, and visceral adhesions
.
After exposure to the hybrid stickleback tapeworm, the authors' analysis found that the degree of fibrosis was positively correlated
with R lineage.
Fibrosis
rarely occurs in G and G backcrossed sticklebacks, regardless of the degree of infection.
The lack of fibrosis in the sea-dwelling sticklebacks and laboratory infections suggests that the sticklebacks have repeatedly evolved
in their fibrosis in freshwater colonization.
Fibrosis is associated
with growth inhibition and elimination of tapeworms.
Fibrosis is a persistent lesion that can persist
long after an immune response has emerged.
R sticklebacks can promote ROS production and fibrosis, both reactions can inhibit tapeworm growth, and the volume of tapeworm in hybrid stickleback F2 is 87.
7%
smaller than that of non-fibrotic sticklebackfish infected tapeworm.
But the production of ROS and fibrosis also comes at the cost
of sticklebacks.
The analysis found that tapeworm infection disrupted female reproductive capacity, and the nesting ability of male sticklebacks with fibrosis was reduced
.
To explore how to balance benefits and harms over evolution, the authors combined quantitative trait locus QTL mapping, population genomics, and transcriptomics
.
The authors genotyped 647 laboratory hybrids F2 stickleback, G stickleback, and R stickleback with 234 information markers, revealing 7 important QTLs that explained tapeworm, fibrosis, granulomas, and ROS changes
.
For example, in ROS QTL on Chr15, the R allele confers higher ROS, but the QTL, R allele on Chr11 reduces ROS
.
Reanalyzing whole-genome sequencing of mixed populations, the authors identified several loci that underwent positive selection in G sticklebacks and others that evolved
in resistant R sticklebacks.
Within fibrotic QTL, the strongest selection targets include the gene SPL1b, which produces the transcription factor PU.
1, which regulates fibroblast polarization and tissue fibrosis
.
Three profibrotic genes, SPL1 STAT6 Cyp3a48, were missing in the evolutionary selection of G sticklebacks, but were not detected in R
.
R sticklebacks will also evolve around
profibrotic TMEM39A and fibrotic-resistant hnf4a.
The two are selected
in opposite directions among the sticklebacks of the two lakes.
This study shows that in repeated selection evolution, different populations have different resistance to tapeworm resistance and fibrosis, resulting in different
parasite prevalence.
These differences are consistent with theoretical models, in which host-parasites co-evolve, replacing steady states, and evolving resistant and tolerant populations
at different costs.
This study also provides a model
for understanding the evolutionary effects of balancing benefits and damage in parasite epidemiology.
| Enzymatic
parasites can increase the pressure of host evolutionary selection and promote immune evolution
.
However, sometimes this selection evolution does not always go in the direction
of increasing resistance.
Resistance-based immune responses can have undesirable consequences that affect host survival and reproduction
by consuming limited resources or inducing autoimmune diseases that reduce host fitness.
Evolutionary optimization theory suggests that evolutionary increased parasite resistance must be balanced
against the cost of immune response.
Only in this way can evolution move in the direction of optimal resistance and immune response
.
Populations may evolve to tolerate, allowing infection to persist while reducing infection mortality and reproductive costs
.
Tolerance itself is expensive and either drains energy to repair damage or allows infection
.
Intraspecific variations in immune costs are rarely studied in a pattern-evolved manner, and there are few models
of tolerance or resistance.
Daniel I.
Bolnick's team from the University of Texas at Austin published an article in Science titled Evolutionary gain and loss of a pathological immune response to parasitism
。 Modelled on sticklebackfish in two lakes, the study explored the effects
of balancing gains and damage in tapeworm infection on the evolution of immune tolerance and resistance populations.
The marine population of the three-spined fish Gasterosteus aculeatus encountered freshwater tapeworms less often and therefore did not evolve resistance
.
Later, marine threefish established populations in freshwater, thus evolving resistance
.
But infection rates also vary from lake to lake, and sometimes prevalence varies
even for similar lakes.
The authors noted that the infection rates of sticklebacks in Lake Roberts and Lake Gaolings (R and G) diverged to 0 and greater than 50%, and the two were located in close
proximity.
The authors hypothesize that differences in infection prevalence reflect the evolution of resistance in R sticklebacks and tolerance in G
sticklebacks.
The authors crossed sticklebacks from R and G and exposed them to schizocephalus tapeworm
.
The analysis found that the infection rate of hybrid sticklebackfish with a large proportion of R was low
.
When tapeworms reach 50 mg, birds come to fish, and birds are the end hosts
of tapeworms.
The growth of tapeworms in the backcrossed sticklebacks is inhibited and does not reach this threshold, protecting the fish from predation
.
The contrast found that R sticklebacks produced more ROS in granulocytes after infection and showed severe peritoneal fibrosis
.
In vertebrates, parasites cause tissue damage, leading to inflammation, fibroblast proliferation, collagen deposition, and visceral adhesions
.
After exposure to the hybrid stickleback tapeworm, the authors' analysis found that the degree of fibrosis was positively correlated
with R lineage.
Fibrosis
rarely occurs in G and G backcrossed sticklebacks, regardless of the degree of infection.
The lack of fibrosis in the sea-dwelling sticklebacks and laboratory infections suggests that the sticklebacks have repeatedly evolved
in their fibrosis in freshwater colonization.
Fibrosis is associated
with growth inhibition and elimination of tapeworms.
Fibrosis is a persistent lesion that can persist
long after an immune response has emerged.
R sticklebacks can promote ROS production and fibrosis, both reactions can inhibit tapeworm growth, and the volume of tapeworm in hybrid stickleback F2 is 87.
7%
smaller than that of non-fibrotic sticklebackfish infected tapeworm.
But the production of ROS and fibrosis also comes at the cost
of sticklebacks.
The analysis found that tapeworm infection disrupted female reproductive capacity, and the nesting ability of male sticklebacks with fibrosis was reduced
.
To explore how to balance benefits and harms over evolution, the authors combined quantitative trait locus QTL mapping, population genomics, and transcriptomics
.
The authors genotyped 647 laboratory hybrids F2 stickleback, G stickleback, and R stickleback with 234 information markers, revealing 7 important QTLs that explained tapeworm, fibrosis, granulomas, and ROS changes
.
For example, in ROS QTL on Chr15, the R allele confers higher ROS, but the QTL, R allele on Chr11 reduces ROS
.
Reanalyzing whole-genome sequencing of mixed populations, the authors identified several loci that underwent positive selection in G sticklebacks and others that evolved
in resistant R sticklebacks.
Within fibrotic QTL, the strongest selection targets include the gene SPL1b, which produces the transcription factor PU.
1, which regulates fibroblast polarization and tissue fibrosis
.
Three profibrotic genes, SPL1 STAT6 Cyp3a48, were missing in the evolutionary selection of G sticklebacks, but were not detected in R
.
R sticklebacks will also evolve around
profibrotic TMEM39A and fibrotic-resistant hnf4a.
The two are selected
in opposite directions among the sticklebacks of the two lakes.
This study shows that in repeated selection evolution, different populations have different resistance to tapeworm resistance and fibrosis, resulting in different
parasite prevalence.
These differences are consistent with theoretical models, in which host-parasites co-evolve, replacing steady states, and evolving resistant and tolerant populations
at different costs.
This study also provides a model
for understanding the evolutionary effects of balancing benefits and damage in parasite epidemiology.
Original link:
http://doi.
org/10.
1126/science.
abo3411
Platemaker: Eleven
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.
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