Transposable elements are not reactivated in natural hybrids of the yeast Saccharomyces paradoxus, but their accumulation is genotype-specific and is not predicted by the evolutionary divergence between a hybrid's parents.

Hybridization barriers in Arabidopsis thaliana can be established by paternally expressed imprinted genes (PEGs) that affect cellularization of the endosperm during seed development.

Xenopus laevis arose from hybridization of two different frog species millions of years ago, leading to adaptation of the genetic networks controlling early embryonic development and stem cell induction to balance expression between the genes inherited from each ancestor.

Hybridization and introgression blur species boundaries and broaden genetic diversity available for adaptation; and widespread introgression underpins the evolution of races of the generalist pathogen Albugo candida that specialise on different host plant species.

Following exposure of Leishmania culture promastigotes to DNA stress, single-cell RNA sequencing reveals discrete clusters of cells associated with efficient generation of hybrids between different species and strains in vitro marked by expression of the ancestral gamete fusogen HAP2.

Genetic barriers to gene flow maintain divergent linked substitution rates in hybridization.

Hybridization not only generates genetic diversity, but this diversity can alter the shape of the fitness landscape, changing which genotypic combinations are favored by natural selection and which accessible genotypic paths lead to novel fitness peaks.

A synthesis of recent hybridization literature reveals emerging patterns in the evolution of genomes after hybridization, processes proposed to explain those patterns, and important open questions to direct future hybrid genomics research.

Unique mechanisms of genetic exchange in the important protozoan pathogen Trypanosome cruzi were characterized in detail using genome analyses of hybrid clones at different time points, showing initial tetraploids followed by genome erosion.

Genomic data for the parasites that cause visceral leishmaniasis provides the first global picture of the diversity and evolution of the pathogen and the epidemiology of this fatal tropical disease.