生命科学最新文献

Soil salinity largely impacts plant growth and development worldwide. Uncovering important regulators involved in plant salt tolerance is crucial for helping plants survive in saline land through genetic engineering. Nonetheless, potential key genes directly related to tolerance to soil salinity have not been fully identified. Through a soil-based genetic screen, we obtained the salinity-tolerant mutant tos1 (tolerance of salt 1), which exhibited glossier and greener leaf morphology under salt stress. tos1 mutation localized at the functionally uncharacterized gene BOUNDARY OF ROP DOMAIN3 (BDR3). A defect in BDR3 results in enhanced resistance to salt stress, accompanied by lower Na⁺ accumulation and water deprivation mediated by a decreased transpiration rate, due to the increased accumulation of cuticular wax, especially VLCFAs and alkanes. BDR3 has no lipase activity, but the fatty acid metabolic process was strongly affected, and glycerolipid hydrolysis was enhanced in tos1; more fatty acids were consumed for wax synthesis, strengthening the cuticular wax maintenance. Our results demonstrate that BDR3 is a novel and negative regulator involved in plant salt tolerance, controlling cuticular transpiration and ion balance depending on its biofunctions in wax synthesis through fatty acid metabolic reprogramming. The study could provide a new molecular basis for the improvement of the regulatory network of wax biosynthesis and plant salt tolerance.

Photoperiod regulates flowering time and maturity in soybean, thereby determining yield performance and latitudinal adaptation. However, the molecular network through which photoperiod regulates flowering remains incompletely elucidated. Here, we identify two BBX family transcription factors, BBX32a and BBX32b, that act as positively regulators flowering under long-day (LD) conditions in soybean. We demonstrate that BBX32a and BBX32b can form both homologous and heterologous dimers. The bbx32a and bbx32b mutants exhibit significantly delayed flowering compared to wild-type W82. However, the bbx32a bbx32b double mutants flower at a similar time to the single mutants, suggesting that the BBX32a-BBX32b heterodimer plays a central role in regulating soybean flowering. E3 and E4 upregulate the transcription of BBX32a and BBX32b, which repress E1 transcription to promote flowering under LD conditions. Genetic evidence demonstrates that BBX32a and BBX32b regulate flowering time, completely dependent on functional E3, E4 and E1 family genes. Four haplotypes of BBX32a were identified in 1295 soybean accessions; BBX32a^Hap3 exhibits significantly reduced nuclear accumulation relative to BBX32a^Hap1. The BBX32a^Hap1 allele is predominantly fixed in cultivated soybeans, whereas BBX32a^Hap2 and BBX32a^Hap3 alleles remain largely unexploited. Collectively, our findings identify novel genetic targets for developing novel soybean cultivars adapted to high-latitude regions, thereby maximising yield potential.

The plant circadian clock synchronizes endogenous rhythms with environmental cues, ensuring optimal growth and development. While the transcription-translation feedback loops (TTFLs) model provides a foundational framework for circadian system, the mechanisms that precisely control the diel and circadian oscillation of key clock genes remain incompletely understood. In particular, the expression of PSEUDO-RESPONSE REGULATOR 9 (PRR9), a dawn-phased core oscillator, needs to be rigorously regulated for proper clock function and environmental responsiveness. Here, we systematically dissected the cis-regulatory architecture of PRR9 promoter using LUC reporter transgenic lines with large-fragment deletions and site-directed mutagenesis. We identified distinct cis-elements that govern PRR9 transcript abundance, rhythmicity and environmental responsiveness. Notably, we discovered a previously uncharacterized 27-bp sequence without any known circadian motifs, which is essential for PRR9 transcriptional rhythmicity, challenging the common view that clock-controlled cis-elements alone determine clock gene expression. These findings refine the TTFLs model and strengthen the link between PRR9 promoter architecture and its role in responding to light and temperature signals to achieve growth advantage.

Silicosis is a progressive occupational lung disease marked by persistent silica-induced inflammation and irreversible pulmonary fibrosis. The NLRP3 inflammasome, an innate immune sensor, has been implicated as a key driver of silica-triggered inflammation and fibrosis in preclinical models. However, the specific role of NLRP3 in immune cells, particularly within myeloid cells (monocytes, macrophages and neutrophils), remains poorly defined. In this study, we investigated the in vivo contribution of myeloid-derived NLRP3 to silica-induced lung pathology using a conditional NLRP3 knockout mouse model (LysM^Cre Nlrp3^fl/fl). These mice exhibited efficient deletion of NLRP3 in both resident and infiltrating lung myeloid cells. Following intranasal delivery of 2 mg of silica, NLRP3 expression was upregulated in myeloid cells by day 3. Despite upregulation of NLRP3 in myeloid cells by day 3, early inflammasome activation in the tissue and BAL, including caspase-1 cleavage and IL-1β and IL-18 secretion, remained intact. During the chronic phase (days 14 and 28), myeloid NLRP3 deletion did not mitigate hallmark features of silicosis, including alveolitis, structural lung damage, airway remodeling or peribronchial alpha-smooth muscle actin expression. Furthermore, the formation and size of silicotic nodules were unaffected. These findings indicate that NLRP3 expression in myeloid cells is not essential for the development of silica-induced pulmonary inflammation, tissue damage or fibrosis. This work highlights the need to explore alternative cellular sources and mechanisms of NLRP3-driven pathology in silicosis.

Wounding in plants elicits immunity and tissue repair, but how these responses are coordinated has yet to be elucidated. While plant metacaspases resemble animal caspases in structure and immunity induction, their role in tissue repair and regeneration is unknown. Using Arabidopsis mutants lacking type II metacaspases AtMC4 or AtMC9, we found that the majority of the highly induced, wound-responsive genes in Arabidopsis thaliana are suppressed by the loss of AtMC4, while AtMC9 plays an auxiliary role in defense activation. Specifically, AtMC4, but not AtMC9, is required for the activation of genes involved in tissue repair, such as the developmental regulator WOX5, as well as for root regeneration from excised leaves. Instead, AtMC9 mediates the repression of a subset of basal immunity genes, which modifies the wound-activated defense response from that induced by molecular patterns such as the bacterial flg22 elicitor. Our results thus reveal a conserved protease module that coordinates plant defense and tissue repair upon wounding. They could be new targets to improve crop performance and plant transformation protocols that involve tissue wounding before transgenic plant selection and regeneration. The groups of genes with distinctive requirements for the two metacaspases could provide markers to dissect how these specialized proteases affect different response pathways that underpin the multifaceted wounding response.

The soybean GmSHMT08 (Rhg4) is a major gene conferring resistance to soybean cyst nematode (SCN), which is a devastating pathogen in soybean, yet its underlying resistance mechanism remains elusive. Heat shock protein 70 (HSP70) mainly functions in maintaining protein homoeostasis and regulating plant immunity. In this study, CRISPR/Cas9-mediated knockout of two highly similar GmHSP70s [GmHSP70-13a (Glyma.13g254900) and GmHSP70-15a (Glyma.15g059900)] enhanced, whereas overexpressing either of them suppressed, SCN resistance. Both GmHSP70-13a and GmHSP70-15a interacted with the key one-carbon metabolism enzyme GmSHMT08, and promoted GmSHMT08 degradation via 26S proteasome pathway, but neither of them altered GmSHMT08 transcript levels in soybean. Furthermore, both GmHSP70-13a and GmHSP70-15a were strongly induced in susceptible soybeans, while both of them still remained low in resistant soybeans, after SCN infection. Taken together, GmSHMT08-mediated SCN resistance is shown to be negatively modulated by both GmHSP70-13a and GmHSP70-15a. The regulation is facilitated through interacting with and influencing 26S proteasome system-involved degradation of GmSHMT08. This study elucidates a SCN-resistance mechanism of GmSHMT08, expands functions of HSP70s and provides two GmHSP70s gene-editing targets for soybean SCN resistance breeding.