https://scholar.dgist.ac.kr/handle/20.500.11750/9984 2026-09-13T08:25:01Z https://scholar.dgist.ac.kr/handle/20.500.11750/60685 Title: Arabidopsis WSS1A, a DNA-protein crosslink repair protease, delays leaf senescence in cooperation with SUMO3 Author(s): Park, Sanghoon; Oh, Hyunwoo; Jeong, Ukcheol; Lee, Jae Ho; Choi, Hyeyoung; Park, Hyunsu; Kim, Jinkwang; Kim, Yongmin; Kwak, Junmin; Yoon, Yeong Seon; Li, Zhonghai; Lee, Jong-Chan; Woo, Hye Ryun Abstract: Leaf senescence, the final stage of leaf development, is regulated by complex interplays of intrinsic genetic programs and environmental cues. Throughout their lifetimes, all living organisms encounter various endogenous and environmental challenges, many of which can cause potentially fatal DNA damage. Among these, DNA-protein crosslinks (DPCs) are particularly deleterious, as they obstruct essential processes such as replication and transcription, thereby compromising genome integrity and ultimately leading to premature aging across species. However, the biological significance of DPCs and their repair mechanisms in leaf senescence remains unexplored. Here, we demonstrate that cis-platin (cis-Pt), a potent DPC inducer, accelerates leaf senescence in Arabidopsis. We reveal that Arabidopsis DPC repair factor WSS1A, a WLM/Spr-T metalloprotease, plays a negative role in leaf senescence induced by cis-Pt treatment, darkness, and leaf age. WSS1A forms nuclear condensates via liquid-liquid phase separation both in vitro and in vivo, which is cooperatively driven by its N-terminal segment and intrinsically disordered region. Mechanistically, WSS1A non-covalently interacts with SMALL UBIQUITIN MODIFIER 3 (SUMO3) through its SUMO-interacting motif and is also covalently SUMOylated by SUMO3. Genetic analysis further reveals that WSS1A and SUMO3 act in the same pathway to control cis-Pt-induced leaf senescence. Together, this study establishes a conceptual framework connecting DPC repair and SUMO3-dependent regulation of WSS1A in modulating leaf senescence in Arabidopsis. 2026-07-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/59140 Title: The chloroplast-targeted long noncoding RNA CHLORELLA mediates chloroplast functional transition across leaf ageing via anterograde signalling Author(s): Kang, Myeong Hoon; Lee, Juhyeon; Kim, Jinkwang; Mohammad, Hazara Begum; Park, Jeehye; Jung, Hyun Ju; Kim, Seonghwan; Lee, Heeho; Yang, Seong Wook; Kwak, June Myoung; Kim, Min-Sik; Lee, Jong-Chan; Lim, Pyung Ok Abstract: The transition from chloroplast biogenesis to degeneration during leaf senescence is critical for plants’ fitness, as it facilitates the relocation of nutrients to reproductive organs1, 2–3. However, it remains largely unknown how the timing of this transition is regulated by the coordination between chloroplasts and the nucleus4,5. Here we describe the regulatory mechanism underlying this transition in Arabidopsis thaliana. CHLOROPLAST-RELATED LONG NONCODING RNA (CHLORELLA) is highly co-expressed with genes supporting chloroplast function during leaf development. Leaves lacking CHLORELLA exhibit precocious senescence and reduced expression of chloroplast-associated genes, suggesting that CHLORELLA helps maintain chloroplast function. Mechanistically, CHLORELLA transcripts are translocated into chloroplasts and contribute to the accumulation of the plastid-encoded RNA polymerase complex. As leaves age, the expression of CHLORELLA decreases, leading to reduced plastid-encoded RNA polymerase accumulation and diminished transcription of photosynthesis-related genes, which may trigger leaf senescence. Moreover, CHLORELLA expression is activated by GOLDEN2-LIKE1 and GOLDEN2-LIKE2, master regulators of chloroplast development6, 7–8. Our study unravels a long-noncoding-RNA-based anterograde signalling mechanism that facilitates timely leaf senescence. © 2025 Elsevier B.V., All rights reserved. 2025-10-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/58662 Title: High-temperature-induced FKF1 accumulation promotes flowering through the dispersion of GI and degradation of SVP Author(s): Lee, Hong Gil; Kim, Jinkwang; Park, Kyung-Ho; Lee, Hongwoo; Kim, Sol-Bi; Jung, Ji-Yul; Gwak, Eunha; Ahn, Ji Hoon; Jung, Jae-Hoon; Lee, Jong-Chan; Seo, Pil Joon Abstract: Floral transition is influenced by photoperiod and ambient temperature, which are integrated to modulate development via a molecular mechanism that remains to be elucidated. Here we demonstrate that the F-box protein FLAVIN-BINDING, KELCH REPEAT, F-BOX 1 (FKF1) and its interacting partner GIGANTEA (GI), central regulators of photoperiodic flowering, target SHORT VEGETATIVE PHASE (SVP) for 26S-proteasome-dependent degradation to regulate the temperature-responsive developmental transition to flowering. At low temperatures, GI is sequestered in liquid-like nuclear condensates. By contrast, FKF1 accumulates at high temperatures and releases GI from condensates to form a nuclear-dispersed FKF1–GI complex, leading to SVP degradation under short-day conditions. Temperature sensitivity is significantly reduced in fkf1-t, gi-2 and fkf1-2 gi-2 mutants. We propose that the FKF1–GI complex mediates the proteolysis of a floral repressor via reversible liquid–liquid phase separation to accelerate floral transition at high temperatures. © The Author(s), under exclusive licence to Springer Nature Limited 2025. 2025-06-30T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/57394 Title: Phytochrome-interacting factors PIF4 and PIF5 directly regulate autophagy during leaf senescence in Arabidopsis Author(s): Lee, Juhyeon; Kang, Myeong Hoon; Choi, Da-Min; Marmagne, Anne; Park, Jeehye; Lee, Heeho; Gwak, Eunha; Lee, Jong-Chan; Kim, Jeong-Il; Masclaux-Daubresse, Celine; Lim, Pyung Ok Abstract: During leaf senescence, autophagy plays a critical role by removing damaged cellular components and participating in nutrient remobilization to sink organs. However, how AUTOPHAGY (ATG) genes are regulated during natural leaf senescence remains largely unknown. In this study, we attempted to identify upstream transcriptional regulator(s) of ATG genes and their molecular basis during leaf senescence in Arabidopsis through the combined analyses of promoter binding, autophagy flux, and genetic interactions. We found that PHYTOCHROME-INTERACTING FACTOR4 (PIF4) and PIF5 directly bind to the promoters of ATG5, ATG12a, ATG12b, ATG8a, ATG8e, ATG8f, and ATG8g, inducing their transcription. These target ATG genes are down-regulated in pif4, pif5, and pif4pif5 mutants, resulting in decreased autophagic activity and slower degradation of chloroplast proteins and chlorophyll. Conversely, overexpression of ATG8 genes accelerated protein degradation with early leaf senescence. Moreover, our data suggested partial suppression of the pif4pif5 phenotype by ATG8a overexpression. PIF4/PIF5 also influence senescence induced by nutrient starvation, another hallmark of the autophagy pathway. Furthermore, we observed that the PIF4/PIF5-ATG regulatory module may contribute to seed maturation. Our study not only unveils transcriptional regulators of autophagy in natural leaf senescence but also underscores the potential role of PIF4/PIF5 as functional regulators in leaf senescence and nutrient remobilization. 2025-01-31T15:00:00Z