Diverse mechanisms contribute to the evolution of reproductive barriers, a process that is critical in speciation. Amongst these are alterations in gene products and in gene dosage that affect development and reproductive success in hybrid offspring. Because of its strict parent-of-origin dependence, genomic imprinting is thought to contribute to the aberrant phenotypes observed in interspecies hybrids in mammals and flowering plants, when the abnormalities depend on the directionality of the cross. In different groups of mammals, hybrid incompatibility has indeed been linked to loss of imprinting. Aberrant expression levels have been reported as well, including imprinted genes involved in development and growth. Recent studies in humans emphasize that genetic diversity within a species can readily perturb imprinted gene expression and phenotype as well. Despite novel insights into the underlying mechanisms, the full extent of imprinted gene perturbation still remains to be determined in the different hybrid systems. Here we review imprinted gene expression in intra- and interspecies hybrids and examine the evolutionary scenarios under which imprinting could contribute to hybrid incompatibilities. We discuss effects on development and reproduction and possible evolutionary implications.
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http://dx.doi.org/10.1038/hdy.2014.11 | DOI Listing |
Mol Biol Rep
January 2025
Federal Research Centre «Fundamentals of Biotechnology», Russian Academy of Sciences, Moscow, Russia, 119071.
Background: TRIM28 plays a crucial role in maintaining genomic stability and establishing imprinting, facilitated by the diversity of KRAB zinc finger proteins. The SUMOylation of TRIM28 is essential for its function and is enhanced in the presence of the KRAB domain. Previously, we demonstrated that Kaiso, another factor capable of interacting with TRIM28, can promote its SUMOylation.
View Article and Find Full Text PDFClin Genet
January 2025
Programa de Pós-graduação em Ciências da Saúde, Universidade de Brasília, Brasília, Brazil.
Silver-Russell Syndrome (SRS) is a genetic disorder characterized by intrauterine and postnatal growth restriction. Most cases are caused by an imprinting error either with hypomethylation of the Imprinted Control Region 1 at 11p15.5, or maternal uniparental disomy of chromosome 7.
View Article and Find Full Text PDFNature
January 2025
School of Biological Sciences, Department of Molecular Biology, University of California, San Diego, La Jolla, CA, USA.
Tissue-resident memory CD8 T (T) cells provide protection from infection at barrier sites. In the small intestine, T cells are found in at least two distinct subpopulations: one with higher expression of effector molecules and another with greater memory potential. However, the origins of this diversity remain unknown.
View Article and Find Full Text PDFNature
January 2025
Department of Neurology, Weill Institute for Neurosciences, University of California San Francisco, San Francisco, CA, USA.
Female mammalian cells have two X chromosomes, one of maternal origin and one of paternal origin. During development, one X chromosome randomly becomes inactivated. This renders either the maternal X (X) chromosome or the paternal X (X) chromosome inactive, causing X mosaicism that varies between female individuals, with some showing considerable or complete skew of the X chromosome that remains active.
View Article and Find Full Text PDFJ Endocr Soc
January 2025
Cellular and Molecular Endocrinology Laboratory LIM/25, Division of Endocrinology and Metabolism, Clinicas Hospital, School of Medicine, University of Sao Paulo, 01246-903 Sao Paulo, Brazil.
Human puberty is a dynamic biological process determined by the increase in the pulsatile secretion of GnRH triggered by distinct factors not fully understood. Current knowledge reveals fine tuning between an increase in stimulatory factors and a decrease in inhibitory factors, where genetic and epigenetic factors have been indicated as key players in the regulation of puberty onset by distinct lines of evidence. Central precocious puberty (CPP) results from the premature reactivation of pulsatile secretion of GnRH.
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