scholarly journals Sexual selection modulates genetic conflicts and patterns of genomic imprinting

Evolution ◽  
2017 ◽  
Vol 71 (3) ◽  
pp. 526-540 ◽  
Author(s):  
Gonçalo S. Faria ◽  
Susana A. M. Varela ◽  
Andy Gardner
Keyword(s):  
Sexual Selection ◽  
Genomic Imprinting ◽  
Genetic Conflicts

Epigenetic regulation of placental endocrine lineages and complications of pregnancy

2013 ◽  
Vol 41 (3) ◽  
pp. 701-709 ◽  
Author(s):  
Rosalind M. John
Keyword(s):  
Genomic Imprinting ◽  
Giant Cells ◽  
In Utero ◽  
Imprinted Genes ◽  
Endocrine Organ ◽  
Fetal Physiology ◽  
Trophoblast Giant Cells ◽  
In Utero Development ◽  
Genetic Conflicts

A defining feature of mammals is the development in utero of the fetus supported by the constant flow of nutrients from the mother obtained via a specialized organ: the placenta. The placenta is also a major endocrine organ that synthesizes vast quantities of hormones and cytokines to instruct both maternal and fetal physiology. Nearly 20 years ago, David Haig and colleagues proposed that placental hormones were likely targets of the epigenetic process of genomic imprinting in response to the genetic conflicts imposed by in utero development [Haig (1993) Q. Rev. Biol. 68, 495–532]. There are two simple mechanisms through which genomic imprinting could regulate placental hormones. First, imprints could directly switch on or off alleles of specific genes. Secondly, imprinted genes could alter the expression of placental hormones by regulating the development of placental endocrine lineages. In mice, the placental hormones are synthesized in the trophoblast giant cells and spongiotrophoblast cells of the mature placenta. In the present article, I review the functional role of imprinted genes in regulating these endocrine lineages, which lends support to Haig's original hypothesis. I also discuss how imprinting defects in the placenta may adversely affect the health of the fetus and its mother during pregnancy and beyond.

scholarly journals Genetic conflicts in genomic imprinting

1998 ◽  
Vol 265 (1413) ◽  
pp. 2393-2397 ◽  
Author(s):  
Austin Burt ◽  
Robert Trivers
Keyword(s):  
Genomic Imprinting ◽  
Genetic Conflicts

Genetic conflicts and the evolutionary origin of genomic imprinting

1999 ◽  
Vol 14 (5) ◽  
pp. 197-201 ◽  
Author(s):  
Hamish G. Spencer ◽  
Andrew G. Clark ◽  
Marcus W. Feldman
Keyword(s):  
Genomic Imprinting ◽  
Evolutionary Origin ◽  
Genetic Conflicts

scholarly journals Genetic Conflicts, Multiple Paternity and the Evolution of Genomic Imprinting

Genetics ◽  
1998 ◽  
Vol 148 (2) ◽  
pp. 893-904
Author(s):  
Hamish G Spencer ◽  
Marcus W Feldman ◽  
Andrew G Clark
Keyword(s):  
Genomic Imprinting ◽  
Multiple Paternity ◽  
The Other ◽  
Growth Inhibitors ◽  
Genetic Conflict ◽  
Quantitative Genetic ◽  
Mean Fitness ◽  
Genetic Conflicts ◽  
Maternal Imprinting ◽  
Over Time

Abstract We present nine diallelic models of genetic conflict in which one allele is imprintable and the other is not to examine how genomic imprinting may have evolved. Imprinting is presumed to be either maternal (i.e., the maternally derived gene is inactivated) or paternal. Females are assumed to be either completely monogamous or always bigamous, so that we may see any effect of multiple paternity. In contrast to previous verbal and quantitative genetic models, we find that genetic conflicts need not lead to paternal imprinting of growth inhibitors and maternal imprinting of growth enhancers. Indeed, in some of our models—those with strict monogamy—the dynamics of maternal and paternal imprinting are identical. Multiple paternity is not necessary for the evolution of imprinting, and in our models of maternal imprinting, multiple paternity has no effect at all. Nevertheless, multiple paternity favors the evolution of paternal imprinting of growth inhibitors and hinders that of growth enhancers. Hence, any degree of multiple paternity means that growth inhibitors are more likely to be paternally imprinted, and growth enhancers maternally so. In all of our models, stable polymorphism of imprinting status is possible and mean fitness can decrease over time. Neither of these behaviors have been predicted by previous models.

The katydid that was: the tananá, stridulation, Henry Walter Bates and Charles Darwin

2014 ◽  
Vol 41 (1) ◽  
pp. 131-140 ◽  
Author(s):  
Claudio J. Bidau
Keyword(s):  
Sexual Selection ◽  
Charles Darwin ◽  
Bush Cricket

The Amazonian bush-cricket or katydid, Thliboscelus hypericifolius (Orthoptera: Tettigoniidae: Pseudophyllinae), called tananá by the natives was reported to have a song so beautiful that they were kept in cages for the pleasure of listening to the melodious sound. The interchange of letters between Henry Walter Bates and Charles Darwin regarding the tananá and the issue of stridulation in Orthoptera indicates how this mysterious insect, which seems to be very rare, contributed to the theory of sexual selection developed by Darwin.

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