scholarly journals Trade-off Between Selection for Dosage Compensation and Masculinization on the Avian Z Chromosome

Genetics ◽  
2012 ◽  
Vol 192 (4) ◽  
pp. 1433-1445 ◽  
Author(s):  
Alison E. Wright ◽  
Hooman K. Moghadam ◽  
Judith E. Mank
2021 ◽  
Vol 70 (3) ◽  
pp. 2362-2377
Author(s):  
Zhanghua Cao ◽  
Xiaodong Ji ◽  
Jue Wang ◽  
Shibing Zhang ◽  
Yancheng Ji ◽  
...  

Nature ◽  
1982 ◽  
Vol 296 (5859) ◽  
pp. 763-766 ◽  
Author(s):  
P. R. Baverstock ◽  
M. Adams ◽  
R. W. Polkinghorne ◽  
M. Gelder

2016 ◽  
Author(s):  
A. Bradley Duthie ◽  
Aline M. Lee ◽  
Jane M. Reid

AbstractInbreeding increases parent-offspring relatedness and commonly reduces offspring viability, shaping selection on reproductive interactions involving relatives and associated parental investment (PI). Nevertheless, theories predicting selection for inbreeding versus inbreeding avoidance and selection for optimal PI have only been considered separately, precluding prediction of optimal PI and associated reproductive strategy given inbreeding. We unify inbreeding and PI theory, demonstrating that optimal PI increases when a female's inbreeding decreases the viability of her offspring. Inbreeding females should therefore produce fewer offspring due to the fundamental trade-off between offspring number and PI. Accordingly, selection for inbreeding versus inbreeding avoidance changes when females can adjust PI with the degree that they inbreed. In contrast, optimal PI does not depend on whether a focal female is herself inbred. However, inbreeding causes optimal PI to increase given strict monogamy and associated biparental investment compared to female-only investment. Our model implies that understanding evolutionary dynamics of inbreeding strategy, inbreeding depression, and PI requires joint consideration of the expression of each in relation to the other. Overall, we demonstrate that existing PI and inbreeding theories represent special cases of a more general theory, implying that intrinsic links between inbreeding and PI affect evolution of behaviour and intra-familial conflict.


2017 ◽  
Vol 14 (4) ◽  
pp. 045011 ◽  
Author(s):  
Matti Gralka ◽  
Diana Fusco ◽  
Stephen Martis ◽  
Oskar Hallatschek

2016 ◽  
Vol 283 (1826) ◽  
pp. 20152857 ◽  
Author(s):  
Alexander Kotrschal ◽  
Niclas Kolm ◽  
Dustin J. Penn

Both the brain and the immune system are energetically demanding organs, and when natural selection favours increased investment into one, then the size or performance of the other should be reduced. While comparative analyses have attempted to test this potential evolutionary trade-off, the results remain inconclusive. To test this hypothesis, we compared the tissue graft rejection (an assay for measuring innate and acquired immune responses) in guppies ( Poecilia reticulata ) artificially selected for large and small relative brain size. Individual scales were transplanted between pairs of fish, creating reciprocal allografts, and the rejection reaction was scored over 8 days (before acquired immunity develops). Acquired immune responses were tested two weeks later, when the same pairs of fish received a second set of allografts and were scored again. Compared with large-brained animals, small-brained animals of both sexes mounted a significantly stronger rejection response to the first allograft. The rejection response to the second set of allografts did not differ between large- and small-brained fish. Our results show that selection for large brain size reduced innate immune responses to an allograft, which supports the hypothesis that there is a selective trade-off between investing into brain size and innate immunity.


Author(s):  
Kaitlyn E. Kortright ◽  
Rachel E. Done ◽  
Benjamin K. Chan ◽  
Valeria Souza ◽  
Paul E. Turner

There is increasing interest in phage therapy as an alternative to antibiotics for treating bacterial infections, especially using phages that select for evolutionary trade-offs between increased phage resistance and decreased fitness traits such as virulence in target bacteria. A vast repertoire of virulence factors allows the opportunistic bacterial pathogen, Shigella flexneri , to invade human gut epithelial cells, replicate intracellularly, and evade host immunity through intercellular spread. It is previously shown that OmpA is necessary for intercellular spread of S. flexneri . We hypothesized that a phage which uses OmpA as a receptor to infect S. flexneri , should select for phage-resistant mutants with attenuated intercellular spread. Here we show that phage A1-1, requires OmpA as a receptor and selects for reduced virulence in S. flexneri . We characterized five phage-resistant mutants by measuring phenotypic changes in various traits: cell-membrane permeability, total lipopolysaccharide (LPS), sensitivity to antibiotics, and susceptibility to other phages. Results separated the mutants into two groups: R1 and R2 phenotypically resembled ompA knockouts, whereas R3, R4 and R5 were similar to LPS-deficient strains. Whole genome sequencing confirmed that R1 and R2 had mutations in ompA , while R3, R4 and R5 showed mutations in LPS inner-core biosynthesis genes gmhA and gmhC . Bacterial plaque assays confirmed that all phage-resistant mutants were incapable of intercellular spread. We concluded that selection for S. flexneri resistance to phage A1-1 generally reduced virulence (i.e. intercellular spread), but this trade-off could be mediated either by mutations in ompA or in LPS-core genes that likely altered OmpA conformation. Author Summary Shigella flexneri is a facultative intracellular pathogen of humans, and a leading cause of bacillary dysentery. With few effective treatments and rising antibiotic resistance in these bacteria, there is increasing interest in alternatives to classical infection management of S. flexneri infections. Phage therapy poses an attractive alternative, particularly if a therapeutic phage can be found that results in an evolutionary trade-off between phage resistance and bacterial virulence. Here, we isolate a novel lytic phage from water collected in Cuatro Cienegas, Mexico that uses the OmpA porin of S. flexneri as a receptor. We use phenotypic assays and genome sequencing to show that phage A1-1 selects for phage-resistant mutants that can be grouped into two categories: OmpA-deficient mutants and LPS-deficient mutants. Despite these underlying mechanistic differences, we confirmed that naturally-occurring phage A1-1 selected for evolved phage resistance that coincided with impaired intercellular spread of S. flexneri in a eukaryotic infection model.


2015 ◽  
Author(s):  
James R Walters ◽  
Thomas J Hardcastle ◽  
Chris Jiggins

The evolution of heterogametic sex chromosome is often ? but not always ? accompanied by the evolution of dosage compensating mechanisms that mitigate the impact of sex-specific gene dosage on levels of gene expression. One emerging view of this process is that such mechanisms may only evolve in male-heterogametic (XY) species but not in female-heterogametic (ZW) species, which will consequently exhibit ?incomplete? sex chromosome dosage compensation. However, some recent results from moths suggest that Lepidoptera (moths and butterflies) may prove to be an exception to this prediction. Here we report an analysis of sex chromosome dosage compensation in Heliconius butterflies, sampling multiple individuals for several different adult tissues (head, abdomen, leg, mouth, and antennae). Methodologically, we introduce a novel application of linear mixed-effects models to assess dosage compensation, offering a unified statistical framework that can estimate effects specific to chromosome, to sex, and their interactions (i.e., a dosage effect). Our results show substantially reduced Z-linked expression relative to autosomes in both sexes, as previously observed in bombycoid moths. This observation is consistent with an increasing body of evidence that at least some species of moths and butterflies possess an epigenetic sex chromosome dosage compensating mechanism that operates by reducing Z chromosome expression in males. However, this mechanism appears to be imperfect in Heliconius, resulting in a modest dosage effect that produces an average 5-20% male-bias on the Z chromosome, depending on the tissue. Strong sex chromosome dosage effects have been previously in a pyralid moth. Thus our results reflect a mixture of previous patterns reported for Lepidoptera and bisect the emerging view that female-heterogametic ZW taxa have incomplete dosage compensation because they lack a chromosome-wide epigenetic mechanism mediating sex chromosome dosage compensation. In the case of Heliconius, sex chromosome dosage effects persist apparently despite such a mechanism. We also analyze chromosomal distributions of sex-biased genes and show an excess of male-biased and a dearth of female-biased genes on the Z chromosome relative to autosomes, consistent with predictions of sexually antagonistic evolution.


2019 ◽  
Vol 67 (4) ◽  
pp. 3026-3039 ◽  
Author(s):  
Ruiyang Duan ◽  
Jingjing Wang ◽  
Chunxiao Jiang ◽  
Yong Ren ◽  
Lajos Hanzo

2019 ◽  
Vol 29 (23) ◽  
pp. 4071-4077.e3 ◽  
Author(s):  
Liuqi Gu ◽  
Patrick F. Reilly ◽  
James J. Lewis ◽  
Robert D. Reed ◽  
Peter Andolfatto ◽  
...  

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