Yongxiu Liu

The Thr445Met substitution in the novel allele med25-5 uncouples seed dormancy from flowering, and MED25 acts as a negative regulator of seed dormancy via the DOG1 and ABA pathways. MED25, a pivotal subunit of the Mediator complex, regulates diverse biological processes, but its role in seed dormancy remains unclear. Here, we identified a novel MED25 allele, med25-5, harboring a Thr445Met substitution in the MD domain, which enhances seed dormancy without affecting flowering time in Arabidopsis thaliana. The med25-5 mutant exhibited increased dormancy with altered expressions in DOG1 and ABA signaling genes (e.g., ABI1, NHL6) and increased sensitivity to ABA and PAC. Either dog1-3 or abi3-10 can completely repress the enhanced seed dormancy of med25, indicating MED25 regulates dormancy requiring the DOG1 and ABA pathways. The Thr445 residue is conserved across crops, highlighting MED25's potential for crop improvement against pre-harvest sprouting. Our study uncovers MED25 as a negative regulator of seed dormancy, providing insights into the molecular mechanisms coordinating dormancy and flowering.

Seed dormancy and germination are crucial processes affecting the propagation and survival of plant populations. These phenomena are precisely regulated through a complex interplay between internal signals, such as plant hormones and environmental cues including light, temperature, moisture, and nutrient availability. Dormancy release and germination initiation are distinct, yet closely associated, processes involving complex transcriptional, translational, and epigenetic changes mediated by intricate regulatory mechanisms. This review comprehensively summarizes the complex regulatory networks governing seed dormancy and germination across different plant species. By integrating physiological, genetic, and molecular biology perspectives, the latest advances in the research on mechanisms regulating seed dormancy and germination are discussed, providing valuable insights for improving seed quality through biotechnology-based breeding strategies and establishing a solid foundation for future research in this field.

SUMMARY: Thousand grain weight (TGW) is one of the most important factors that control grain weight and crop yield. To date, dozens of wheat genes related to TGW have been isolated; however, the underlying molecular mechanisms governing grain development in wheat ( Triticum aestivum ) remain largely unknown. Benefiting from whole‐genome resequencing and genome‐wide association study, we identified an R2R3‐type myeloblastosis (MYB) transcription factor, TaODORANT1, which was tightly associated with TGW. TaODORANT1 was specifically and highly expressed during the wheat grain developing stage. Knockout of TaODORANT1 led to an increase in TGW and starch content, as well as affected the expression of starch synthesis‐related genes. Loss of function of TaODORANT1 altered the molecular structure and physiochemical properties of grain starch. Haplotype analysis showed that favorable Hap IV of TaODORANT1‐A and favorable Hap I of TaODORANT1‐B were significantly associated with the production of larger grains and higher TGW, respectively. Moreover, TaODORANT1 was a crucial targeted gene continuously selected in wheat domestication and breeding, and its orthologous genes might have retained similar functions in response to grain development. Our results highlight the importance of TaODORANT1 in affecting TGW, presenting potential targets for improving yield in wheat.

Background: Seed dormancy and size are two crucial traits influencing crop yield, and they have undergone strong selection during cereal domestication and improvement. However, the genetic basis underlying the antagonistic effects between seed dormancy and seed size remains poorly understood. Results: Based on genome-wide association study, we perform a comprehensive comparative analysis of 545 global wheat accessions to dissect the genetic architecture of these two traits during wheat improvement. We detect a strong negative correlation between the accumulation of favorable alleles for seed dormancy and the accumulation of favorable alleles for seed size. At the wheat genome level, a set of SNPs harboring antagonistic alleles explain up to 26.56% and 47.21% of the phenotypic variation for seed dormancy and seed size, respectively. In contrast, a set of SNPs with synergistic alleles account for only 0.54% and 1.12% of the variation in both traits. During wheat breeding improvement, favorable alleles associated with increased seed size are preferentially selected, resulting in a compromise in seed dormancy. Under different climate conditions, the frequencies of haplotypes of the pleiotropic genes with antagonistic effects and synergistic loci collectively shape wheat diversity through balancing seed dormancy and seed size. Conclusions: Our findings reveal the genetic architecture underlying the observed weakening of seed dormancy as seed size increases during wheat improvement, enabling further genome-informed cultivar breeding to balance and improve seed dormancy and seed size traits.

Autophagy and apoplastic ascorbic acid (AsA) play important roles in plant drought tolerance. However, the trans-plasma membrane transport of AsA and its association with autophagy during drought stress are unclear. Here we report an AsA-induced autophagy pathway in plants, wherein plasma-membrane-located cytochrome b561 and DOMON domain (CYBDOM) proteins play positive roles. CYBDOM proteins from the resurrection plant Boea hygrometrica (BhDB) and Arabidopsis (AtDB1) can transport electrons across the plasma membrane using intracellular AsA as an electron donor and apoplastic monodehydroascorbic acid or Fe³⁺ as electron acceptors in Xenopus laevis oocytes. Increased apoplastic AsA, autophagy and drought tolerance are observed in BhDB- and AtDB1-overexpressing Arabidopsis compared with the wild type. CYBDOM proteins interact with respiratory burst oxidase homologue D (RbohD), which serves as the adaptor to bind autophagy related gene 8 protein (ATG8) and cargo protein for autophagic degradation. AsA increases AtDB1 protein level and its interaction with RbohD. Together, the AsA-activated CYBDOM–RbohD synergy to induce autophagy suggests a novel mechanism in plant drought and desiccation tolerance.

Lesion mimicry typically manifests as leaf disease–like symptoms in the absence of pathogen infection, characterized by a hypersensitive response, which is intricately linked to plant disease resistance. In this study, the wheat (Triticum aestivum L.) mutant lesion mimic 34 (lm34), harboring a recessive mutation in the Zhongyou 206 (ZY206) background, was comprehensively investigated. The lm34 mutation was mapped to a 140-kb region on chromosome 4AL through bulked segregant exome capture sequencing and fine-mapping. Sequence comparison and phenotypic analysis of the lm34Jing mutant revealed that TraesCS4A03G1225400, encoding a typical coiled coil–nucleotide-binding–leucine-rich repeat protein, is the causal gene in lm34. Transient expression assays in Nicotiana benthamiana leaves indicated that the TaLM34 extended coiled coil domain can induce cell death. Furthermore, lm34 mutants display elevated reactive oxygen species levels and significantly increased expression of pathogenesis-related (PR) genes (PR2 and PR10), leading to enhanced powdery mildew resistance. Our findings suggest that TaLM34 can serve as a potential target for the development of wheat cultivars with improved disease resistance. Overall, our study sheds light on the molecular mechanisms underlying wheat disease resistance and cell death.

The origin of genes from non-coding sequences is a long-term and fundamental biological question. However, how de novo genes originate and integrate into the existing pathways to regulate phenotypic variations is largely unknown. Here, we selected seven genes from 782 de novo genes for functional exploration based on transcriptional and translational evidence. Subsequently, we revealed that SWK, a de novo gene that originated from a non-coding sequence in Arabidopsis thaliana, plays a role in seed germination under osmotic stress. SWK is primarily expressed in dry seed, imbibing seed and silique. SWK can be fully translated into an 8 kDa protein, which is mainly located in the nucleus. Intriguingly, SWK was integrated into an extant pathway of hydrogen peroxide content (folate synthesis pathway) via the upstream gene cytHPPK/DHPS, an Arabidopsis-specific gene that originated from the duplication of mitHPPK/DHPS, and downstream gene GSTF9, to improve seed germination in osmotic stress. In addition, we demonstrated that the presence of SWK may be associated with drought tolerance in natural populations of Arabidopsis. Overall, our study highlights how a de novo gene originated and integrated into the existing pathways to regulate stress adaptation.

Main conclusion WOX family gene WOX2 is highly expressed during seed development, which functions redundantly with WOX1 and WOX4 to positively regulate seed germination. Abstract WOX (WUSCHEL-related homeobox) is a family of transcription factors in plants. They play essential roles in the regulation of plant growth and development, but their function in seed germination is not well understood. In this report, we show that WOX1, WOX2, and WOX4 are close homologues in Arabidopsis. WOX2 has a redundant function with WOX1 and WOX4, respectively, in seed germination. WOX2 is highly expressed during seed development, from the globular embryonic stage to mature dry seeds, and its expression is decreased after germination. Loss of function single mutant wox2, and double mutants wox1 wox2 and wox2 wox4-1 show decreased germination speed. WOX2 and WOX4 are essential for hypocotyl–radicle zone elongation during germination, potentially by promoting the expression of cell wall-related genes. We also found that WOX2 and WOX4 regulate germination through the gibberellin (GA) pathway. These results suggest that WOX2 and WOX4 integrate the GA pathway and downstream cell wall-related genes during germination.

Main conclusion Taetr1-1 can promote enhanced seed dormancy and ethylene insensitivity in wheat, indicating a conserved function of ETR1 in regulating seed dormancy. Abstract Lots of wheat cultivars have weak dormant seed. Weak seed dormancy can cause pre-harvest sprouting (PHS) in grain which significantly reduces grain yield and quality. The mining of causal genes of PHS resistance will serve to enhance breeding selection and cultivar development. In a previous study in Arabidopsis, we identified reduced dormancy 3 as a loss-of-function mutant of the ethylene receptor 1 (ETR1), which can control seed dormancy through the ERF12–TPL–DOG1 pathway. However, it is unknown whether ETR1 also functions in the regulation of wheat seed dormancy. To identify the regulatory role of ETR1 in wheat, we cloned TaETR1 and overexpressed the gain-of-function mutant Taetr1-1. The result indicated that overexpression of Taetr1-1 can promote enhanced seed dormancy and ethylene insensitivity in wheat. This study contributed to our understanding of the molecular basis for the regulation of wheat PHS resistance.

SUMMARY: Seed dormancy is an important adaptive trait to prevent germination occurring at an inappropriate time. The mechanisms governing seed dormancy and germination are complex. Here, we report that FACTOR INTERACTING WITH POLY(A) POLYMERASE 1 (FIP1), a component of the pre‐mRNA 3′ end processing machinery, is involved in seed dormancy and germination processes in Arabidopsis thaliana. FIP1 is mainly expressed in seeds and the knockout of FIP1 causes reduced seed dormancy, indicating that FIP1 positively influences seed dormancy. Meanwhile, fip1 mutants are insensitive to exogenous ABA during seed germination and early seedling establishment. The terms ‘seed maturation’ and ‘response to ABA stimulus’ are significantly enriched in a gene ontology analysis based on genes differentially expressed between fip1‐1 and the wild type. Several of these genes, including ABI5, DOG1 and PYL12, show significantly decreased transcript levels in fip1. Genetic analysis showed that either cyp707a2 or dog1‐5 partially, but in combination completely, represses the reduced seed dormancy of fip1, indicating that the double mutant cyp707a2 dog1‐5 is epistatic to fip1. Moreover, FIP1 is required for CFIM59, another component of pre‐mRNA 3′ end processing machinery, to govern seed dormancy and germination. Overall, we identified FIP1 as a regulator of seed dormancy and germination that plays a crucial role in governing these processes through the DOG1 and ABA pathways.