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Li Yin

Publications and source records attributed to Li Yin.

2 recordsLinked to original sources

A CqbZIP55-CqPIF3 regulatory module associated with light-responsive flavonoid biosynthesis during quinoa seedling de-etiolation.

Quinoa (Chenopodium quinoa) is an emerging leafy vegetable and microgreen crop rich in health-promoting flavonoids, yet the regulatory mechanisms linking light perception to early metabolic adaptation remain unclear. Here, we integrated phenotypic, transcriptomic, metabolomic, and molecular analyses to investigate early de-etiolation responses in quinoa seedlings. Short-term light exposure rapidly promoted seedling establishment and induced transcriptional programs associated with photosynthesis, carbon metabolism, hormone signaling, and flavonoid biosynthetic gene expression, whereas metabolite changes were more limited, indicating temporal uncoupling between transcriptional activation and metabolic accumulation. Genome-wide bZIP analysis identified CqbZIP55 as a light-responsive regulator that directly binds and activates the CqCHS promoter. CqPIF3 also bound the CqCHS promoter and showed stronger transactivation activity than CqbZIP55 in transient reporter assays. Protein interaction and dual-luciferase assays showed that CqbZIP55 physically interacts with CqPIF3 and modulates CqPIF3-associated promoter activity. Exogenous quercetin upregulated CqbZIP55 and prolonged CqCHS expression, suggesting a candidate metabolite-associated reinforcement mechanism. Together, these findings support functional interplay between CqbZIP55 and CqPIF3 in light-responsive regulation of flavonoid biosynthetic gene expression in quinoa seedlings, while further quinoa-based perturbation and in vivo promoter-occupancy assays are required to establish their physiological role in planta. This study provides a framework for further investigation of photoprotective metabolic regulation in quinoa.

Chenopodium quinoa

MYDGF as a telomerase activator and therapeutic target for osteoarthritis.

Osteoarthritis (OA) involves progressive cartilage breakdown. This is driven by impaired chondrocyte function and an imbalance in the extracellular matrix homeostasis. However, the key upstream regulators that maintain healthy chondrocytes are still not fully known. Here, we report that myeloid-derived growth factor (MYDGF) is a novel regulator of telomerase activity and is critical for cartilage health. Using a genome-wide CRISPR-Cas9 screen with a TERT reporter system, MYDGF was identified as a strong positive regulator of telomerase. Functional studies confirmed that MYDGF positively regulates TERT expression and telomerase activity in both HeLa and ATDC5 cells. In a mouse surgical destabilization of the medial meniscus (DMM) OA model, MYDGF knockout (KO) mice exhibited more severe cartilage damage. Conversely, delivering MYDGF into the knee joint using AAV virus partially alleviated cartilage injury. Transcriptome profiling revealed that MYDGF-deficient chondrocytes exhibit downregulated key pathways involved in matrix building and upregulated inflammatory signals, indicating a shift in cell state. In summary, our work establishes MYDGF as a key upstream factor for both telomerase and cartilage matrix homeostasis remodeling. It connects telomerase function to chondrocyte health. These findings also highlight MYDGF as a promising new target for treating osteoarthritis.

Cartilage degeneration