Genetic diversity in the threatened Bellevalia webbiana (Asparagaceae) parallels functional and reproductive traits

Amongst the numerous Italian narrow endemic plants, the Webb’s hyacinth (Bellevalia webbiana Parl., Asparagaceae) is one of the most evolutionarily relevant, and threatened. The range of this bulbous perennial herb is restricted to an area of pre-Apennines (100–700 m a.s.l.) in Tuscany, and Emilia-Romagna (Central Italy), with two disjunct population groups. Typical habitats for Webb’s hyacinth are open fields, and meadows, wood margins, olive groves, and vineyards. During the last century, Webb’s hyacinth disappeared from several historical localities due to the development of human settlements. For these reasons, this species is currently listed in The IUCN Red List of Threatened Species as Endangered (EN A2c). Despite contributions providing important information on the species’ reproductive and functional traits, no population genetic information was available so far. In this study, a DNA fingerprinting approach was applied to study the five richest populations of this species (each with N > 50 individuals): three in Tuscany (Pratolino, Uccellatoio, Tavarnuzze), and two in Emilia-Romagna (Casola Valsenio and Faenza)

Genetic differentiation among populations of the threatened Bellevalia webbiana (Asparagaceae) and its consequence on conservation

The narrow central Italian endemic and threatened Webb’s hyacinth (Bellevalia webbiana), a perennial herb, is a clear example of a species that has disappeared from several localities due to the development of human settlements. We characterized population genetics of this species to infer possible threats to its viability. We used a dominant DNA fingerprinting approach to infer genetic relationships among the five richest populations known for this species (each with N > 50 individuals). We highlighted phenomena of genetic erosion, with values of intrapopulation-gene-diversity quite similar across all populations (mean value 0.113), but a mean F st value only slightly below the mean found in other plant species using similar approaches. Despite an overall genetic similarity among populations, a population from Faenza (Emilia-Romagna) is clearly separated from all the others on genetic grounds, and may be defined as an Evolutionarily Significant Unit, worth of special conservation attention. Interestingly, this latter population is also behaving differently from all the others in terms of both vegetative and reproductive functional strategies. Our results highlight the relevance of evolutionary approaches to conservation biology for preserving a genetic diversity linked to local adaptations

Threshold-controlled ubiquitination of the EGFR directs receptor fate

How the cell converts graded signals into threshold-activated responses is a question of great biological relevance. Here, we uncover a nonlinear modality of epidermal growth factor receptor (EGFR)-activated signal transduction, by demonstrating that the ubiquitination of the EGFR at the PM is threshold controlled. The ubiquitination threshold is mechanistically determined by the cooperative recruitment of the E3 ligase Cbl, in complex with Grb2, to the EGFR. This, in turn, is dependent on the simultaneous presence of two phosphotyrosines, pY1045 and either one of pY1068 or pY1086, on the same EGFR moiety. The dose-response curve of EGFR ubiquitination correlate precisely with the non-clathrin endocytosis (NCE) mode of EGFR internalization. Finally, EGFR-NCE mechanistically depends on EGFR ubiquitination, as the two events can be simultaneously re-engineered on a phosphorylation/ubiquitination-incompetent EGFR backbone. Since NCE controls the degradation of the EGFR, our findings have implications for how the cell responds to increasing levels of EGFR signalling, by varying the balance of receptor signalling and degradation/attenuation

USP9X Controls EGFR Fate by Deubiquitinating the Endocytic Adaptor Eps15

Following activation by its cognate ligand(s), the epidermal growth factor receptor (EGFR) is rapidly routed to the lysosome for degradation in a ubiquitination-dependent fashion. This pathway represents the major mechanism of long-term attenuation of EGFR signaling, and its deregulation is a significant feature in different types of cancers. Here we demonstrate, through a systematic RNAi-based approach, that several deubiquitinating (DUB) enzymes extend or decrease EGFR half-life upon EGF stimulation. We focus on USP9X, whose depletion severely affects EGFR turnover, interfering with its internalization and trafficking. We identify the endocytic protein Eps15 as one of the critical substrates of USP9X, and we map the Eps15 ubiquitination sites. We found that Eps15 monoubiquitination occurs already at minimal dose of EGF stimulation and is essential for EGFR internalization. Overall, our findings identify USP9X as a novel regulator of EGFR endocytosis and suggest a model whereby cycles of ubiquitination and deubiquitination events on endocytic accessory proteins may regulate the internalization and trafficking of the EGFR toward the lysosomes. Savio et al. undertook a siRNA screen to find 18 DUBs that affect EGFR degradation. They focus on USP9X, whose depletion significantly delayed EGFR internalization and trafficking. USP9X counteracts monoubiquitination of Eps15 that occurs at minimal EGF dose and is critical for EGFR internalization