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Lijie Zhang

Publications and source records attributed to Lijie Zhang.

2 recordsLinked to original sources

The transcription factors GmBBX17 and GmSTFs antagonistically regulate shade avoidance in soybean by oppositely modulating GmSRG1 transcription.

High-density planting represents a promising strategy to enhance crop productivity. However, this agronomic practice inevitably triggers shade avoidance responses, manifested as stem and petiole elongation, suppressed branching, and altered petiole angles. Elucidating the molecular underpinnings of shade avoidance remains imperative for rationalizing planting density strategies in crop production. Here, we report that soybean SHADE-REDUCED GENE 1 (GmSRG1) inhibits the stem and petiole growth both in white light and low ratio of Red:Far-red light conditions in soybean. GmSRG1 likely represents a catalytically inactive homolog of xyloglucan endotransglucosylase/hydrolase that lacks the conserved active site. Despite its enzymatic deficiency, it is associated with enhanced xyloglucan-degrading activity and prevents xyloglucan accumulation in soybean. GmBBX17 binds to the GmSRG1 promoter to repress its transcription, whereas GmSTFs (GmSTF1 and GmSTF2) transcriptionally activate GmSRG1. GmBBX17 physically interacts with GmSTFs to antagonistically regulate GmSRG1 expression. Unlike GmSRG1, its close homolog GmXTH23 is associated with increased xyloglucan accumulation and reduced xyloglucan-degrading activity, while GmSRG1 physically interacts with GmXTH23 and counteracts this GmXTH23-associated effect. Our work reveals an integrated regulatory network comprising the GmBBX17-GmSTFs transcriptional module and the GmSRG1-GmXTH23 regulatory module, which collectively govern shade avoidance architecture in soybean.

Glycine max

Integrating clinical and genomic features to predict response to neoadjuvant therapy in microsatellite-stable rectal cancer.

BACKGROUND: Neoadjuvant therapy (NAT) has shifted rectal cancer management toward organ preservation. However, achieving a complete response (CR) for "watch-and-wait" strategies is hindered by high response heterogeneity. Although immunotherapy-combined NAT has expanded the candidate pools, the predictive significance of molecular alterations remains unclear. OBJECTIVES: This study aimed to evaluate clinical and genomic profiles of rectal cancer patients undergoing NAT to identify response predictors and to develop a nomogram for estimating CR probability. DESIGN: Retrospective, single-center cohort study. METHODS: This study included 437 patients with rectal adenocarcinoma at Fudan University Shanghai Cancer Center between December 2019 and March 2023. Patients underwent paired tumor and germline genomic sequencing (887-gene panel) before NAT. Logistic and Cox regression analyses were performed to identify clinical and genetic risk factors associated with tumor response and long-term survival. RESULTS: Of the 437 patients, 96.6% had microsatellite-stable (MSS) tumors. In the MSS locally advanced rectal cancer cohort (N = 307), the CR rate was 35.5%. Multivariate analysis identified immunotherapy-combined NAT (iTNT) (OR 4.41, 95% CI: 2.42-8.27), SYNE1 mutation (OR 2.12, 95% CI: 1.06-4.26), negative mesorectal fascia (MRF) status (OR 0.34, 95% CI: 0.17-0.66), and lower tumor location (OR 0.48, 95% CI: 0.27-0.84) as independent predictors of CR. KRAS mutation was the sole independent predictor of reduced disease-free survival (DFS; HR 1.93, 95% CI: (1.11-3.36), p = 0.020). KRAS G12D subtype was associated with the worst 2-year distant metastasis-free survival (71.3%) and exhibited a distinct predilection for lung metastasis. The clinical-genomic nomogram yielded strong discrimination (AUC = 0.705) and calibration, with favorable DCA net benefit. CONCLUSION: Clinical and genomic features jointly determine outcomes in MSS rectal cancer. SYNE1 mutation serves as a novel biomarker for CR, while KRAS mutations, especially the G12D subtype, identify patients at high risk for systemic relapse. The clinical-genomic nomogram facilitates individualized selection for organ-preservation strategies.

biomarker