BackgroundPlants respond to abiotic stress on physiological, biochemical and molecular levels. This includes a global change in their cellular proteome achieved by changes in the pattern of their protein synthesis and degradation. The ubiquitin-proteasome system (UPS) is a key player in protein degradation in eukaryotes. Proteins are marked for degradation by the proteasome by coupling short chains of ubiquitin polypeptides in a three-step pathway. The last and regulatory stage is catalyzed by a member of a large family of substrate-specific ubiquitin ligases.ResultsWe have identified AtPUB46 and AtPUB48—two paralogous genes that encode ubiquitin ligases (E3s)—to have a role in the plant environmental response. The AtPUB46, −47, and −48 appear as tandem gene copies on chromosome 5, and we present a phylogenetic analysis that traces their evolution from an ancestral PUB-ARM gene. Single homozygous T-DNA insertion mutants of AtPUB46 and AtPUB48 displayed hypersensitivity to water stress; this was not observed for similar mutants of AtPUB47. Although the three genes show a similar spatial expression pattern, the steady state levels of their transcripts are differentially affected by abiotic stresses and plant hormones.Conclusions AtPUB46 and AtPUB48 encode plant U-Box E3s and are involved in the response to water stress. Our data suggest that despite encoding highly homologous proteins, AtPUB46 and AtPUB48 biological activity does not fully overlap.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-016-0963-5) contains supplementary material, which is available to authorized users.

The structure and connectivity of protein-protein interaction (PPI) networks are maintained throughout evolution by coordinated changes (coevolution) of network proteins. Despite extensive research, relatively little is known regarding the molecular basis and functional implications of the coevolution of PPI networks. Here, we used proliferating cell nuclear antigen, a hub protein that mediates DNA replication and repair in eukaryotes, as a model system to study the coevolution of PPI networks in fungi. Using a combined bioinformatics and experimental approach, we discovered that PCNA-partner interactions tightly coevolved in fungal species, leading to specific modes of recognition. We found that fungal proliferating cell nuclear antigen-partner interaction networks diverged into two distinct groups as a result of such coevolution and that hybrid networks of these groups are functionally noncompatible in Saccharomyces cerevisiae. Our results indicate that the coevolution of PPI networks can form functional barriers between fungal species, and thus can promote and fix speciation.interdomain connecting loop | yeast two hybrid | directed evolution P rotein-protein interaction (PPI) networks play vital roles in executing almost all essential biological processes. The availability of sequencing data, as well as high-throughput experimental approaches to identify and generate comprehensive maps of PPIs, has enabled the development of a network-based view of biological processes (1, 2). Such networks are composed of ensembles of proteins that act together in a coordinated manner to execute a variety of essential biological processes, such as DNA replication, transcription, and signal transduction. In many cases, such networks are modular and contain highly connected proteins, termed "hub proteins," that can regulate a given biological process by switching partners with high spatial and temporal resolution (3).Many PPI networks are conserved over evolutionary time scales to promote a variety of biological processes in different organisms (4). One mechanism to maintain network structure and connectivity throughout evolution involves the coevolution of interacting proteins through coordinated changes in protein-protein interfaces (5). The coevolution of interacting proteins can form reproductive barriers between organisms as a result of hybrid network incompatibility, and thus can be an important driving force in promoting and fixing speciation. Currently, the study of coevolution of PPI networks is extremely challenging because of difficulties in identifying and characterizing coordinated sequence changes in network proteins during natural evolution. Even if such sequence changes are detected, their functional implications are difficult to predict. Thus, relatively little is known overall regarding the dynamics and functional importance of the coevolution of hubpartner interactions across different species.In eukaryotes, DNA replication and repair processes are mediated by proliferating cell nuclear antigen (PCNA) throug...

Novel regenerative therapies may stem from deeper understanding of the mechanisms governing cardiovascular lineage diversification. Using enhancer mapping and live imaging in avian embryos, and genetic lineage tracing in mice, we investigated the spatio-temporal dynamics of cardiovascular progenitor populations. We show that expression of the cardiac transcription factor Nkx2.5 marks a mesodermal population outside of the cardiac crescent in the extraembryonic and lateral plate mesoderm, with characteristics of hemogenic angioblasts. Extra-cardiac Nkx2.5 lineage progenitors migrate into the embryo and contribute to clusters of CD41+/CD45+ and RUNX1+ cells in the endocardium, the aorta-gonad-mesonephros region of the dorsal aorta and liver. We also demonstrated that ectopic expression of Nkx2.5 in chick embryos activates the hemoangiogenic gene expression program. Taken together, we identified a hemogenic angioblast cell lineage characterized by transient Nkx2.5 expression that contributes to hemogenic endothelium and endocardium, suggesting a novel role for Nkx2.5 in hemoangiogenic lineage specification and diversification.DOI: http://dx.doi.org/10.7554/eLife.20994.001

Novel regenerative therapies may stem from deeper understanding of the mechanisms governing cardiovascular lineage diversification. Using enhancer mapping and live imaging in avian embryos, and genetic lineage tracing in mice, we investigated the spatio-temporal dynamics of cardiovascular progenitor populations. We show that expression of the cardiac transcription factor Nkx2.5 marks a mesodermal population outside of the cardiac crescent in the extraembryonic and lateral plate mesoderm, with characteristics of hemogenic angioblasts. Extra-cardiac Nkx2.5 lineage progenitors migrate into the embryo and contribute to clusters of CD41 + /CD45 + and RUNX1 + cells in the endocardium, the aorta-gonad-mesonephros region of the dorsal aorta and liver. We also demonstrated that ectopic expression of Nkx2.5 in chick embryos activates the hemoangiogenic gene expression program. Taken together, we identified a hemogenic angioblast cell lineage characterized by transient Nkx2.5 expression that contributes to hemogenic endothelium and endocardium, suggesting a novel role for Nkx2.5 in hemoangiogenic lineage specification and diversification.