Genetic analysis combined with whole genome sequencing elucidates mechanisms and pathways that form and prevent a specific class of genome rearrangements, foldback inversions, seen in many human cancers.

Evolutionary reduction in tissue number involves the simplification of the seaming process but not signaling during epithelial fusion.

Rapid acquisition of chromosome rearrangements, together with independently acting transmission distorter alleles on each chromosome, drive near complete sterility in fission yeast hybrids.

Proximity and homology guided inter-chromosomal translocations drive karyotype evolution.

African haplotypes of a meiotic drive supergene in Drosophila melanogaster called Segregation Distorter show signs of a recent selective sweep, reduced recombination, and increased genetic load.

Complex chromosomal rearrangements similar to those described in cancer and developmental syndromes occur in plants during postzygotic genome elimination, a centromeric-derived incompatibility.

Through the interaction between PCP signaling and N-cadherin, oriented cell division and cell rearrangement are coordinated to establish the appropriate tissue architecture critical for limb skeletal morphogenesis.

A method to generate human cells with massive chromosomal aberrations on a specific chromosome allows analysis of their consequences.

Emx2 is not required for sibling HCs to acquire their designated locations within the neuromast, inferring that Emx2 mediates opposite HC orientation by changing location of hair bundle establishment.

In addition to its academic merits, characterizing the genetic determinants of male (in)fertility and identifying clinically actionable genetic variants can lead to improved diagnosis or even treatment of such conditions.