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Parental sex discrimination and intralocus sexual conflict

Patten, Manus M.; Haig, David
Fonte: The Royal Society Publicador: The Royal Society
Tipo: Artigo de Revista Científica
Relevância na Pesquisa
Intralocus sexual conflict occurs when populations segregate for alleles with opposing fitness consequences in the two sexes. This form of selection is known to be capable of maintaining genetic and fitness variation in nature, the extent of which is sensitive to the underlying genetics. We present a one-locus model of a haploid maternal effect that has sexually antagonistic consequences for offspring. The evolutionary dynamics of these maternal effects are distinct from those of haploid direct effects under sexual antagonism because the relevant genes are expressed only in females. Despite this, we find the same opportunity for sexually antagonistic polymorphism at the maternal effect locus as at a direct effect locus. Thus, sexually antagonistic maternal effects may underlie some natural genetic variation. The model we present permits alternative interpretations of how the genes are expressed and how the fitness variation is assigned, which invites a theoretical comparison to models of both imprinted genes and sex allocation.

The evolution of X chromosome inactivation in mammals: the demise of Ohno’s hypothesis?

Pessia, Eugénie; Engelstädter, Jan; Marais, Gabriel A. B.
Fonte: Springer Publicador: Springer
Tipo: Artigo de Revista Científica
Publicado em /04/2014 ENG
Relevância na Pesquisa
Ohno's hypothesis states that dosage compensation in mammals evolved in two steps: a twofold hyperactivation of the X chromosome in both sexes to compensate for gene losses on the Y chromosome, and silencing of one X (X-chromosome inactivation, XCI) in females to restore optimal dosage. Recent tests of this hypothesis have returned contradictory results. In this review, we explain this ongoing controversy and argue that a novel view on dosage compensation evolution in mammals is starting to emerge. Ohno's hypothesis may be true for a few, dosage-sensitive genes only. If so few genes are compensated, then why has XCI evolved as a chromosome-wide mechanism? This and several other questions raised by the new data in mammals are discussed, and future research directions are proposed.; Agence Nationale de la Recherche grant number: (ANR-12-BSV7-0002), Instituto Gulbenkian de Ciência.