Nature Plants最新文献

Vacuoles are essential for cellular metabolism and growth and the maintenance of internal turgor pressure. They sequester lytic enzymes, ions and secondary metabolites that, if leaked into the cytosol, could lead to cell death. Despite their pivotal roles, quality control pathways that safeguard vacuolar integrity have remained elusive in plants. Here we describe a conserved vacuolar quality control pathway that is activated upon cell wall damage in a turgor-pressure-dependent manner. Cell wall perturbations induce a distinct modification—ATG8ylation—on the vacuolar membrane (tonoplast) that is regulated by the V-ATPase and ATG8 conjugation machinery. Genetic disruption of tonoplast ATG8ylation impairs vacuolar integrity, leading to cell death. Together, our findings reveal a homeostatic pathway that preserves vacuolar integrity upon cell wall damage.

During male germline development, microspores divide asymmetrically into a larger vegetative cell and a smaller generative cell. This pollen mitosis I is followed by a second, symmetric division of the generative cell to form two sperm nuclei in which the cell cycle is arrested in the G1 phase until fertilization. It is known that the R2R3 MYB transcription factor DUO1 is required for PMII, and that duo1 mutants arrest in the S phase before division. DUO1 is transcriptionally controlled by AT-RICH INTERACTING DOMAIN-CONTAINING PROTEIN 1 (ARID1) and can additionally be influenced by microRNAs at the mRNA level. In contrast to the control of PMII entry by DUO1, the mechanism by which divisions after PMII are prevented is not well understood.

The researchers focus on RBR1 as its animal homologue is known to associate with ARID transcription factors. Indeed, Li and colleagues used reciprocal co-immunoprecipitation assays to confirm that RBR1 interacts with ARID1. As rbr1 knockout mutants are gametophytic lethal, the authors isolated the hypomorphic allele rbr1-4, which produces a 3ʹ truncated transcript that leads to an unstable protein lacking part of the C terminus. Although rbr1-4 mutants clearly have reproductive defects, this phenotype does not correlate with overproliferation but rather underproliferation of germ cells, resulting in a higher proportion of pollen containing only a single sperm nucleus. The authors show that RBR1 interacts with DUO1 in an ARID1-dependent way, and that this interaction stabilizes DUO1. As DUO1 protein levels are reduced in rbr1-4 mutants despite higher transcript levels, it can be assumed that the extreme C terminus of RBR1 is required to stabilize DUO1. These findings suggest that RBR1 is required to promote PMII together with ARID1 and DUO1. Interestingly, it has previously been reported that a stronger rbr1 mutant allele causes overproliferation of germ cells, suggesting that RBR1 might also be required to repress further divisions after PMII. Therefore, it is tempting to speculate that DUO1 requires stabilization by RBR1 to coordinate PMII with a mechanism that prevents additional divisions thereafter.

Cell plate formation in plants is a complex process orchestrated by the targeted delivery of Golgi-derived and endosomal vesicles containing cell plate components to the phragmoplast midzone. It has long been hypothesized that vesicles are directionally transported along phragmoplast microtubules by motor proteins. However, the mechanisms governing the accumulation and immobilization of vesicles at the phragmoplast midzone remain elusive, and the motor protein responsible has yet to be identified. Here we show that the plant-specific class II kinesin-12 (kinesin12-II) functions as a motor protein that drives vesicle transport towards the phragmoplast midzone in the moss Physcomitrium patens. In the kinesin12-II mutant, the directional movement of cell plate materials towards the midzone and their retention were abolished, resulting in delayed cell plate formation and phragmoplast disassembly. A macroscopic phenotype arising from kinesin12-II disruption was the impediment to gametophore development. We showed that this defect was attributable to the production of aneuploid and polyploid cells in the early gametophore, where chromosome missegregation and cytokinesis failure occurred. These findings suggest that plant kinesin-12 has evolved to acquire a unique and critical function that facilitates cell plate formation in the presence of phragmoplasts.

Legumes form root nodules with symbiotic nitrogen-fixing rhizobacteria, which require ample iron to ensure symbiosis establishment and efficient nitrogen fixation. The functions and mechanisms of iron in nitrogen-fixing nodules are well established. However, the role of iron and the mechanisms by which legumes sense iron and incorporate this cue into nodulation signalling pathways remain unclear. Here we show that iron is a key driver of nodulation because symbiotic nodules cannot form without iron, even under conditions of sufficient light and low nitrogen. We further identify an iron optimum for soybean nodulation and the iron sensor BRUTUS A (BTSa) which acts as a hub for integrating iron and nodulation cues. BTSa is induced by rhizobia, binds to and is stabilized by iron. In turn, BTSa stabilizes and enhances the transcriptional activation activity of pro-nodulation transcription factor NSP1a by monoubiquitination from its RING domain and consequently activates nodulation signalling. Monoubiquitination of NSP1 by BTS is conserved in legumes to trigger nodulation under iron sufficiency. Thus, iron status is an essential cue to trigger nodulation and BTSa integrates cues from rhizobial infection and iron status to orchestrate host responses towards establishing symbiotic nitrogen fixation.

The nuclear pore complex (NPC) is a cornerstone of eukaryotic cell functionality, orchestrating the nucleocytoplasmic shuttling of macromolecules. Here we report that Plant Nuclear Envelope Transmembrane 1 (PNET1), a transmembrane nucleoporin, is an adaptable NPC component that is mainly expressed in actively dividing cells. PNET1’s selective incorporation into the NPC is required for rapid cell growth in highly proliferative meristem and callus tissues in Arabidopsis. We demonstrate that the cell cycle-dependent phosphorylation of PNET1 coordinates mitotic disassembly and post-mitotic reassembly of NPCs during the cell cycle. PNET1 hyperphosphorylation disrupts its interaction with the NPC scaffold, facilitating NPC dismantling and nuclear membrane breakdown to trigger mitosis. In contrast, nascent, unphosphorylated PNET1 is incorporated into the nuclear pore membrane in the daughter cells, where it restores interactions with scaffolding nucleoporins for NPC reassembly. The expression of the human PNET1 homologue is required for and markedly upregulated during cancer cell growth, suggesting that PNET1 plays a conserved role in facilitating rapid cell division during open mitosis in highly proliferative tissues.

Pepper (Capsicum spp.) is a widely consumed vegetable with exceptionally large genomes in Solanaceae, yet its genomic evolutionary history remains largely unknown. Here we present 11 high-quality Capsicum genome assemblies, including two gap-free genomes, covering four wild and all five domesticated pepper species. We reconstructed the ancestral karyotype and inferred the evolutionary trajectory of peppers. The expanded and variable genome sizes were attributed to differential transposable element accumulations, which shaped 3D chromatin architecture and introduced mutations associated with traits such as fruit orientation and colour. Using a chromatin accessibility atlas of Capsicum, we highlight the influence of transposable elements on regulatory element evolution. Furthermore, by constructing a haploblock map of 124 pepper core germplasms, we uncover frequent introgressions that facilitate the formation of sweet blocky pepper and the acquisition of important traits such as resistance to pepper mild mottle virus. These findings on the genomic and functional evolution of Capsicum will benefit pepper breeding.