Yue Wang

Key message Our study revealed that SlTCP16 can transcriptional activation and interaction with Sl4CL3, thereby enhancing the tomato’s resistance to Pst DC3000. This resistance is associated with an increased accumulation of lignin. Abstract Lignin deposition serves as a critical physical barrier against bacterial pathogens. However, the precise regulatory networks orchestrating this defense response in tomato remain incompletely understood. We identify the transcription factor SlTCP16 as a novel positive regulator of tomato immunity against Pseudomonas syringae pv. tomato (Pst DC3000). We show that Pst DC3000 infection strongly induces SlTCP16 expression. Functionally, SlTCP16 overexpression significantly reduced reactive oxygen species (ROS) accumulation and bolstered disease resistance, while SlTCP16 knockout mutants showed the opposite performance. Mechanistically, we uncover a dual regulatory mode, SlTCP16 not only directly activates the transcription of the lignin biosynthetic gene Sl4CL3 by binding to its promoter but also physically interacts with the Sl4CL3 protein. Sl4CL3 acts downstream of SlTCP16, and overexpression of Sl4CL3 enhanced disease resistance in the sltcp16 mutant. Collectively, our data suggest that SlTCP16 contributes to disease resistance by regulating Sl4CL3 through transcriptional activation and protein-protein interaction. This regulatory module is associated with increased lignin accumulation.

Seed size affects seed vigor, seedling establishment, and seed utilization in tomato. Yet the genetic basis of this trait remains poorly defined in tomato itself. Here, we describe a stable small–seed mutant, T31, isolated from an ethyl methanesulfonate (EMS)–mutagenized population of the elite inbred line DL5. Relative to the wild type, T31 showed a 24% reduction in seed width, whereas vegetative growth and major fruit traits were largely unchanged. Throughout this study, ‘seed size’ refers to seed width, which was used as the principal index of seed size because tomato seeds are oblate. Genetic analysis of six populations (P₁, P₂, F₁, F₂, BC₁, and BC₂) indicated that the phenotype is controlled by a single recessive locus, designated ssm. Bulked segregant analysis sequencing (BSA–seq) placed ssm within a 1.77 –Mb interval on chromosome 4. KASP–based fine mapping reduced this interval to 390 kb and identified six EMS–type SNPs. Only one of these SNPs was located in an exon of Solyc04g073950.2, where it caused a Pro337Ser substitution. This gene encodes a VQ motif–containing protein and was designated SlVQ10. To test gene function, we generated CRISPR/Cas9 knockout lines in the DL5 background. Two independent homozygous knockout lines reproduced the small–seed phenotype. Seed size was reduced by 31–33%, and thousand–seed weight decreased by 33–35%. Histological analysis further showed reduced seed–coat cell expansion in the mutants. Together, the genetic and genome–editing data support SlVQ10 as the gene underlying ssm and indicate that it promotes seed size in tomato.

Previously, research has primarily focused on how the environment affects fruit quality, but there is a lack of studies investigating the impact of different growth stages on fruit quality. In this study, a total of 192 differentially abundant metabolites and 5546 differentially expressed genes were categorized into eight modules exhibiting distinct trends, along with an additional module that remained unchanged throughout all growth stages. These modules elucidate the primary metabolic alterations and transcriptional regulatory networks underlying quality variations in tomato fruits at the mature stage across different growth stages (Spike1–Spike3). Furthermore, an investigation was conducted on the module that remained constant throughout the growth stages. It was observed that the soluble sugar content remained stable across the different growth stages, whereas the levels of total phenols and flavonoids exhibited significant variation. Additionally, the principal metabolites influencing tomato flavor—namely aspartic acid, glutamic acid, glucose, fructose, citric acid, α-linolenic acid, and linoleic acid—did not demonstrate significant changes in content. The findings of this study provide novel insights into the formation of tomato quality and establish a theoretical foundation for the cultivation of long-season tomatoes with stable fruit quality.

Low light stress can aggravate the occurrence of plant bacterial diseases. However, how the basic leucine zipper (bZIP) family regulates the synergistic regulatory network induced by low light stress and pathogen infection at the transcriptional level is still unclear. In this study, we identified SlbZIP17, which has a dual response to Pseudomonas syringae pv. tomato DC3000 ( Pst DC3000) and low light conditions. It revealed that SlbZIP17 reduces tomato ( Solanum lycopersicum ) disease symptoms by activating the positive regulator gene SlβCA3 of Pst DC3000 and increasing the ability of plants to scavenge reactive oxygen species (ROS). Further studies revealed that SlbZIP17 forms a heterodimer with SlMYC2 to synergistically amplify the transcriptional activation effect on SlβCA3 . Moreover, under low light stress, SlHY5 was inhibited, which directly reduced SlbZIP17 and SlβCA3 expression. This process led to a decrease in the interaction of SlbZIP17 and SlMYC2, which reduced the ability of the transcription complex to activate SlβCA3 and thereby increasing the severity of disease symptoms induced by Pst DC3000. These findings offer insights into the mechanism underlying the low light stress–pathogen interaction and provide new targets for improving resistance in tomato varieties for facility cultivation agriculture.

Studies on how SlPR5 genes are involved in Pst DC3000 disease resistance response are lacking. Here, 27 members of the tomato SlPR5 gene family were identified and analyzed. Analysis of conserved structural domains and promoter structure revealed that SlPR5 family members are structurally conserved and contain a variety of antidisease and antistress response elements. We screened out SlPR5-3, which was significantly upregulated, through an analysis of the expression pattern of Pst DC3000 in tomato after inoculation. We generated SlPR5-3 mutants via CRISPR/Cas9 gene editing and SlPR5-3-overexpressing tomato plants to elucidate the function of this gene. The results showed that the SlPR5-3 overexpression lines had reduced lesions, significantly lower pathogen counts, and significantly higher activity indexes of defense-related enzymes, while the mutant lines showed the opposite, indicating that the SlPR5-3 gene positively regulates the immune response against Pst DC3000 in tomato. In this study, we systematically mined and analyzed the tomato SlPR5 family genes, screened out the important genes in this family for the regulation of Pst DC3000 disease resistance, and verified the disease resistance regulatory function of SlPR5-3, laying the foundation for the theoretical study of tomato Pst DC3000 disease resistance and providing a new molecular target for the future breeding of tomato disease resistance.