The Plant Journal最新文献

COP1 is the essential protein that integrates various environmental and hormonal cues to control plant growth and development at multiple levels. COP1 is a RING-finger-type E3 ubiquitin ligase that acts as a potent repressor of photomorphogenesis and flowering by targeting numerous substrates for ubiquitination and promoting their proteolysis via the 26S proteasome system. The WD40 repeat domain with conserved amino acid residues was shown to be essential for interacting with its targets. However, the role of these amino acids in regulating hypocotyl growth and flowering in response to varying light and temperatures remains unknown. Here, we show that tryptophan amino acid at the position 467 residue (COP1^W467) is relevant in mediating the interaction with its targets to regulate the COP1-mediated proteolysis. The COP1^W467 plays a critical role in inducing growth responses in shade light by interacting and degrading HY5, a crucial negative regulator of shade-avoidance response (SAR). Moreover, COP1^W467 integrates warm ambient temperature signals to promote hypocotyl growth by increasing PIF4 and decreasing HY5 protein stability. Finally, we found that COP1^W467 is important in inhibiting flowering under a short-day photoperiod, likely through interacting with CO for degradation. Together, this study highlights that the COP1^W467 residue is essential to regulate seedling photomorphogenesis, SAR, thermomorphogenesis and flowering for the fine adjustment of plant growth and development under dynamic light and temperature conditions.

Melatonin is a pivotal bioactive molecule that enhances plant cold stress tolerance, but the precise mechanisms remain enigmatic. Here, we have discovered that overexpressing melatonin biosynthetic gene ClCOMT1 or applying exogenous melatonin activates the C-repeat binding factor (CBF)-responsive pathway and enhances watermelon cold tolerance. This enhancement is accompanied by elevated levels of nitric oxide (NO) and hydrogen sulfide (H₂S), along with upregulation of nitrate reductase 1 (ClNR1) and L-cysteine desulfhydrase (ClLCD) genes involved in NO and H₂S generation respectively. Conversely, knockout of ClCOMT1 exhibits contrasting effects compared to its overexpression. Furthermore, application of sodium nitroprusside (SNP, a NO donor) and NaHS (a H₂S donor) promotes the accumulation of H₂S and NO, respectively, activating the CBF pathway and enhancing cold tolerance. However, knockout of ClNR1 or ClLCD abolished melatonin-induced H₂S or NO production respectively and abrogated melatonin-induced CBF pathway and cold tolerance. Conversely, supplementation with SNP and NaHS restored the diminished cold response caused by ClCOMT1 deletion. Additionally, deletion of either ClNR1 or ClLCD eliminated NaHS- or SNP-induced cold response, respectively. Overall, these findings suggest a reciprocal positive-regulatory loop between ClNR1-mediated NO and ClLCD-mediated H₂S, which plays a crucial role in mediating the melatonin-induced enhancement of cold tolerance.

Reynoutria japonica Houtt. (Polygonaceae), a traditional Chinese medicine, is one of the top 100 most destructive invasive species worldwide due to its aggressive growth and strong adaptability. Here, we report an 8.04 Gb chromosome-scale assembly of R. japonica with 88 chromosomes across eight homologous sets. Through a combined phylogenetic and genomic analysis, we demonstrate that R. japonica is a mixed auto-/allooctoploid (AAAABBBB). Subgenome A (SubA) exhibited a close phylogenetic relationship with the related species Fallopia multiflora. We also unveiled the origin and evolutionary history of octoploid R. japonica based on resequencing data from Reynoutria species with different ploidy. Comparative genomics analysis revealed the genetic basis of R. japonica's invasivity and adaptability. The auxin response factor (ARF) gene family was significantly expanded in R. japonica, and these genes were highly expressed in rhizomes. We also investigated the collaboration and differentiation of the duplicated genes resulting from auto- and allo-polyploidization at the genomic variation, gene family evolution, and gene expression levels in R. japonica. Transcriptomic analysis of stem internodes and apices at different developmental stages revealed that the octuplication and significant expansion of the SAUR19 and SAUR63 subfamilies due to tandem replication in SubA, and the high expression of these genes in stems, likely contribute to the rapid growth of R. japonica. Our study provides important clues into adaptive evolution and polyploidy dominant traits in invasive plants, and will also provide important guidance for the breeding of polyploid crops.

Plant CSN5 is widely recognized as the subunit of the COP9 signalosome and CSN5 is mainly involved in plant growth and development, and tolerance to biotic and abiotic stresses. However, the molecular mechanism of CSN5 regulating anthocyanin biosynthesis in plants is still largely unknown. Here, we identified FvCSN5 from the woodland strawberry yeast two-hybrid library using the anthocyanin pathway inhibitor MYB1 as bait. We demonstrated the interaction of FvCSN5 and FvMYB1 by H2Y, Pull-down, LCI, and BiFC assays. FvCSN5 was expressed in all test tissues and localized in the nucleus and cytosol with self-activation activity. Stable overexpression of FvCSN5 in woodland strawberries reduced anthocyanin accumulation in fruits. The protein level of FvMYB1 greatly decreased in overexpressing FvCSN5 plants compared with wild-type plants. Protein degradation assay and MG-132 treatment (a proteasome inhibitor blocking 26S proteasome activity) revealed FvCSN5 degraded FvMYB1 through the ubiquitination pathway. In addition, FvCSN5 also interacted with the anthocyanin activator FvBBX20 and FvBBX20 could be degraded by FvCSN5. Moreover, transient expression analysis showed the expression of anthocyanin biosynthetic genes FvCHS and FvF3H was greatly increased and decreased when FvCSN5 was co-expressed with FvMYB1 and FvBBX20, respectively. These results indicate that FvMYB1-FvCSN5-FvBBX20 is a novel ternary complex that regulates anthocyanin biosynthesis by the ubiquitination pathway.

Potassium (K) is a prevalent limiting factor in terrestrial ecosystems, with approximately one-eighth of the world's soils undergoing K⁺ deficiency stress. Upon encountering K⁺ deficiency stress, leaf area (LA) declines before the net photosynthetic rate (A_n). The sequential alterations fundamentally represent the adaptive trade-off between survival and growth in plants subjected to K⁺ deficiency stress. This trade-off is hypothesized to be linked to the differences in the subcellular distribution of limited K⁺ resources. Thus, the K⁺ distribution and apparent concentration in subcellular compartments, along with the LA and A_n characteristics of rapeseed leaves at various developmental stages and K⁺ supply conditions were quantified to elucidate the mechanisms by which subcellular K⁺ regulates leaf growth and survival. The results revealed that during the early stages of K⁺ deficiency, leaves actively downregulate growth to sustain normal physiological functions. This is primarily accomplished by lowering the K⁺ distribution and apparent concentration in vacuoles, restricting LA expansion, and enhancing K⁺ distribution to chloroplasts to ensure A_n. Prolonged K⁺ deficiency decreased the apparent K⁺ concentration in chloroplasts below the critical threshold (37.8 mm), disrupting chloroplast structure and function, impairing A_n, and ultimately threatening the survival of rapeseed. Hence, sustaining an adequate concentration of K⁺ within chloroplasts is crucial for preserving leaf photosynthetic efficiency and ensuring survival under K⁺ deficiency stress. In conclusion, under K⁺ deficiency stress, leaves regulate LA and A_n by trade-offs in the K⁺ distribution between vacuoles and chloroplasts to coordinate growth and survival.