Brown planthopper (Nilaparvata lugens, BPH) is a major pest that severely limits rice production. Although plant defense against BPH involves complex metabolic and structural responses, the role of non-protein amino acids (NPAAs) in this process remains poorly understood. Here, we demonstrate that (R)-β-tyrosine functions as a key defense metabolite that enhances rice resistance to BPH. Exogenous application and genetic manipulation across different rice backgrounds revealed that (R)-β-tyrosine does not directly affect insect survival but instead acts through host-mediated mechanisms. Transcriptomic, histological, and physiological analyses showed that (R)-β-tyrosine promotes the expression of phenylpropanoid pathway genes, leading to increased lignin accumulation, enhanced mechanical strength, and reinforced physical barriers that restrict BPH feeding. Mechanistically, we identify the JA-inducible transcription factor OsMYB72 as a key activator of OsTAM1, the enzyme catalyzing β-tyrosine biosynthesis, thereby linking JA signaling to (R)-β-tyrosine accumulation. This JA-OsMYB72-OsTAM1 module coordinates β-tyrosine production with downstream phenylpropanoid metabolism, promoting lignin deposition and reinforcing structural defense against BPH. Together, our findings establish a link between NPAA metabolism and lignin-associated structural defense, offering insight into metabolite mediated plant resistance to piercing-sucking herbivores.

The piercing-sucking pest, brown planthopper (Nilaparvata lugens, BPH), poses a severe and persistent threat to rice in China and across Asia. During feeding, BPHs secrete salivary proteins to form salivary sheaths, which are crucial for successful and sustained phloem sap ingestion. These salivary sheath proteins are crucial for rice-BPH interactions and hold promise as targets for pest control strategies like RNAi. However, the specific functions of salivary proteins in sheath formation remain largely unclear. In this study, we identify NlSRP, a serine-rich salivary protein in BPH, as a novel planthopper-specific secreted salivary protein. NlSRP is highly expressed in the salivary glands and is delivered into host rice plants during feeding. RNAi-mediated knockdown of NlSRP significantly impairs feeding ability, survival and fecundity of BPH. NlSRP is required for the formation of elongated and branched salivary sheaths in BPH. These results demonstrate that NlSRP plays an essential role in BPH salivary sheath formation, feeding and population growth, advancing our mechanistic understanding of piercing-sucking insect feeding and highlighting its potential as an RNAi-based target for BPH control.

Prostate cancer (PCa) is one of the most common malignancies in men, and sarcosine has been identified as a potential metabolic biomarker for PCa progression. Herein, we develop a ratiometric CdTe quantum dots (R-QDs)/Ag[+] switch-on fluorescent sensing platform for sensitive and specific detection of sarcosine in prostate cancer cells. In this ratiometric design, the 640 nm emission of R-QDs serves as the internal reference signal, while the 520 nm emission is the responsive signal. The sensing strategy is based on Ag[+]-induced quenching of the 520 nm emission (turn-off state), followed by enzymatic recovery of the 520 nm emission via H2O2 generated from sarcosine oxidase-catalyzed oxidation of sarcosine (turn-on state), while the 640 nm reference emission remains essentially unchanged. Under optimal conditions, the nanosensor exhibits a linear response to sarcosine concentration in the range of 0-20 µM with a detection limit of 1.2 µM. The platform demonstrates excellent selectivity toward sarcosine over other interfering substances. Moreover, the nanosensor successfully detects endogenous sarcosine in prostate cancer cell lysates (PC-3 and LNCaP) with significantly higher FL520/FL640 ratio recovery compared to benign prostate epithelial cells (BPH-1). This work provides a cost-effective and reliable tool for sarcosine detection in prostate cancer research.