Evidence for sympatric speciation by host shift in the sea

The genetic divergence and evolution of new species within the geographic range of a single population (sympatric speciation) contrasts with the well-established doctrine that speciation occurs when populations become geographically isolated (allopatric speciation). Although there is considerable theoretical support for sympatric speciation [1, 2], this mode of diversification remains controversial, at least in part because there are few well-supported examples [3]. We use a combination of molecular, ecological, and biogeographical data to build a case for sympatric speciation by host shift in a new species of coral-dwelling fish (genus Gobiodon). We propose that competition for preferred coral habitats drives host shifts in Gobiodon and that the high diversity of corals provides the source of novel, unoccupied habitats. Disruptive selection in conjunction with strong host fidelity could promote rapid reproductive isolation and ultimately lead to species divergence. Our hypothesis is analogous to sympatric speciation by host shift in phytophagous insects [4, 5] except that we propose a primary role for intraspecific competition in the process of speciation. The fundamental similarity between these fishes and insects is a specialized and intimate relationship with their hosts that makes them ideal candidates for speciation by host shift

The recurrent postzygotic pathogenic variant p.Glu47Lys in RHOA causes a novel recognizable neuroectodermal phenotype

RHOA is a member of the Rho family of GTPases that are involved in fundamental cellular processes including cell adhesion, migration, and proliferation. RHOA can stimulate the formation of stress fibers and focal adhesions and is a key regulator of actomyosin dynamics in various tissues. In a Genematcher-facilitated collaboration, we were able to identify four unrelated individuals with a specific phenotype characterized by hypopigmented areas of the skin, dental anomalies, body asymmetry, and limb length discrepancy due to hemihypotrophy of one half of the body, as well as brain magnetic resonance imaging (MRI) anomalies. Using whole-exome and ultra-deep amplicon sequencing and comparing genomic data of affected and unaffected areas of the skin, we discovered that all four individuals carried the identical RHOA missense variant, c.139G>A; p.Glu47Lys, in a postzygotic state. Molecular modeling and in silico analysis of the affected p.Glu47Lys residue in RHOA indicated that this exchange is predicted to specifically alter the interaction of RHOA with its downstream effectors containing a PKN-type binding domain and thereby disrupts its ability to activate signaling. Our findings indicate that the recurrent postzygotic RHOA missense variant p.Glu47Lys causes a specific mosaic disorder in humans