Biology subjects

Ahn, J.-Y.

Publications and source records attributed to Ahn, J.-Y..

3 recordsLinked to original sources

bioRxiv2026

Global Sesame Germplasm Harbors Untapped Genetic Potential for Crop Improvement

Background Sesame (Sesamum indicum L.) is one of the oldest oilseed crops. Its seeds accumulate lignans and antioxidants that determine their nutritional value. Global demand for sesame is rising rapidly, but climate change increasingly threatens sesame yields and seed quality. Here, we analyzed a worldwide panel of 300 sesame accessions to explore the genetic basis of key adaptive and quality traits, specifically flowering time, seed lignan content, and seed antioxidant capacity. Results Whole-genome resequencing revealed previously unreported genetic diversity, expanding the resources available for sesame breeding. By integrating k-mer-based genome-wide association analysis with a graph-based sesame genome, we identified structural variants associated with differences in flowering time and lignan accumulation. A 9.4-kb deletion on chromosome 6 that disrupted SIN_1018434 (an ortholog of Arabidopsis PHOTOPERIOD-INDEPENDENT EARLY FLOWERING 1) and a 6.2-kb Copia-type retrotransposon insertion upstream of SIN_1004470 on chromosome 11 were associated with early flowering. The intact alleles at both loci were associated with delayed flowering and were predominant in low-latitude accessions. High seed lignan content was associated with non-synonymous mutations and copy number variants in glycosyl hydrolase genes on chromosome 6 and an 8.2-kb deletion spanning SIN_1019378 on chromosome 13. Association signals for seed antioxidant traits coincided with loci involved in abiotic stress responses and seed-coat pigmentation. Conclusions These findings highlight the importance of exploring diverse germplasm to uncover previously unrecognized adaptive and quality-associated genomic variation. The loci identified here provide molecular targets for developing climate-adapted cultivars with improved seed quality.

genomics↗

bioRxiv2026

Chemical activation of mitophagy via the N-degron pathway alleviates mitochondrial neuropathies

Pharmacological activation of mitophagy offers a promising strategy to eliminate dysfunctional mitochondria. We previously identified the autophagy receptor p62/SQSTM1 as an N-recognin whose activity is enhanced by Arg/N-degrons. Here, we show that Arg/N-degrons generated by ATE1-encoded R-transferase regulate p62-mediated mitophagy by promoting its recruitment to damaged mitochondria. Structural modification of Arg/N-degrons yielded ATB1071, a 443.5-Da orally bioavailable compound that activates p62 and induces stress-selective mitophagy through both Parkin-independent pathways involving NIPSNAP1 and NIPSNAP2, and a Parkin-dependent pathway involving the substrate EBP1/PA2G4. In Ndufs4-/- mice, a Leigh syndrome (LS) model, ATB1071 induced mitophagy in the brain and exerted therapeutic benefits by reducing neuroinflammation, improving muscle strength and neuromuscular coordination, and extending lifespan. In cerebral ischemia-reperfusion (IR) model mice, ATB1071 reduced infarct volume and neuronal death, and ameliorated multiple behavioral deficits through EBP1-dependent mitophagy. Pharmacokinetic (PK) and toxicological analyses support ATB1071 as a preclinical candidate for mitochondria-associated neurological injury.

cell biology↗

bioRxiv2022

Exploration of mechanisms of drug resistance by polyaneuploid cancer cells in a microfluidic device and patient tissues

Chemoresistance is a major cause of treatment failure in many cancers. However, the life cycle of cancer cells as they respond to and survive environmental and therapeutic stress is understudied. In this study, we utilized a microfluidic device to induce the development of doxorubicin-resistant (DOXR) cells from triple negative breast cancer (TNBC) cells within 11 days by generating gradients of DOX and medium. In vivo chemoresistant xenograft models, an unbiased genome-wide transcriptome analysis, and a patient data/tissue analysis all showed that chemoresistance arose from failed epigenetic control of the nuclear protein-1 (NUPR1)/histone deacetylase 11 (HDAC11) axis, and high Nupr1 expression correlated with poor clinical outcomes. These results suggest that the chip can rapidly induce resistant cells that increase tumor heterogeneity and chemoresistance, highlighting the need for further studies on the epigenetic control of the NUPR1/HDAC11 axis in TNBC.

cancer biology↗