Ning Bai
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Ning Bai has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
Fangren Peng
State Key Laboratory for Development and Utilization of Forest Food Resources, Co-Innovation Center for Sustainable Forestry in Southern China, Nanjing Forestry University , Nanjing, 210037
1 shared publication- Hanqi Huang
State Key Laboratory for Development and Utilization of Forest Food Resources, Co-Innovation Center for Sustainable Forestry in Southern China, Nanjing Forestry University , Nanjing, 210037
1 shared publication - Jiancan Du
CAS Key Laboratory of Tropical Plant Resources and Sustainable Use, Xishuangbanna Tropical Botanical Garden, Chinese Academy of Sciences , Kunming, Yunnan 650223
1 shared publication - Juping Zhang
CAS Key Laboratory of Tropical Plant Resources and Sustainable Use, Xishuangbanna Tropical Botanical Garden, Chinese Academy of Sciences , Kunming, Yunnan 650223
1 shared publication - Kunrong He
State Key Laboratory of Tree Genetics and Breeding, Co-Innovation Center for Sustainable Forestry in Southern China, Jiangsu Key Laboratory for Poplar Germplasm Enhancement and Variety Improvement, Nanjing Forestry University , Nanjing 210037
1 shared publication - Lijuan Zhou
State Key Laboratory of Tree Genetics and Breeding, Co-Innovation Center for Sustainable Forestry in Southern China, Jiangsu Key Laboratory for Poplar Germplasm Enhancement and Variety Improvement, Nanjing Forestry University , Nanjing 210037
1 shared publication
Latest Publications
- 18 June 2026
- Published by Oxford University Press (OUP) in Plant Physiology
- Vol. 201 (3)
Arabidopsis MYC2–ARF16–ABI5 complex functions as a transcriptional switch to regulate jasmonate, auxin, and abscisic acid signaling synergy
Seed germination and post-germination growth are strictly regulated by phytohormones. In Arabidopsis thaliana, jasmonate (JA) and auxin suppress these processes by boosting abscisic acid (ABA) signaling. However, whether there exists a transcriptional switch orchestrating the intricate interplay among these hormones and the underlying molecular mechanisms remain elusive. Herein, we demonstrated that endogenous JA signaling, involving the CORONATINE INSENSITIVE1 (COI1)–JASMONATE ZIM-DOMAIN (JAZ) module and the downstream MYC2, MYC3, and MYC4 transcription factors, potentiates auxin-induced ABA responses. MYC2, MYC3, and MYC4 interact with AUXIN RESPONSE FACTOR10 (ARF10) and ARF16. Consistently, MYC2 and ARF16 synergistically augment ABA signaling-delayed seed germination. Furthermore, MYC2 and MYC4 form a protein complex with ABSCISIC ACID INSENSITIVE5 (ABI5), a master activator of ABA signaling. Genetic analyses suggested that MYC2 positively facilitates ABA responses largely through ABI5. Notably, MYC2 collaborates with ARF16 to enhance the transcriptional activity and protein abundance of ABI5. Intriguingly, MYC2, ARF16, and ABI5 assemble into a ternary complex. Simultaneously disrupting MYC, ARF10/ARF16, and ABI5 renders the seed germination process insensitive to combined JA, auxin, and ABA. Collectively, our findings unveil the MYC–ARF10/ARF16–ABI5 module as a pivotal molecular switch that integrates JA, auxin, and ABA signaling pathways, thereby enabling plants to mount adaptive responses to challenging environmental conditions.
- 18 June 2026
- Published by Oxford University Press (OUP) in Plant Physiology
- Vol. 201 (3)
Arabidopsis MYC2–ARF16–ABI5 complex functions as a transcriptional switch to regulate jasmonate, auxin, and abscisic acid signaling synergy
Seed germination and post-germination growth are strictly regulated by phytohormones. In Arabidopsis thaliana, jasmonate (JA) and auxin suppress these processes by boosting abscisic acid (ABA) signaling. However, whether there exists a transcriptional switch orchestrating the intricate interplay among these hormones and the underlying molecular mechanisms remain elusive. Herein, we demonstrated that endogenous JA signaling, involving the CORONATINE INSENSITIVE1 (COI1)–JASMONATE ZIM-DOMAIN (JAZ) module and the downstream MYC2, MYC3, and MYC4 transcription factors, potentiates auxin-induced ABA responses. MYC2, MYC3, and MYC4 interact with AUXIN RESPONSE FACTOR10 (ARF10) and ARF16. Consistently, MYC2 and ARF16 synergistically augment ABA signaling-delayed seed germination. Furthermore, MYC2 and MYC4 form a protein complex with ABSCISIC ACID INSENSITIVE5 (ABI5), a master activator of ABA signaling. Genetic analyses suggested that MYC2 positively facilitates ABA responses largely through ABI5. Notably, MYC2 collaborates with ARF16 to enhance the transcriptional activity and protein abundance of ABI5. Intriguingly, MYC2, ARF16, and ABI5 assemble into a ternary complex. Simultaneously disrupting MYC, ARF10/ARF16, and ABI5 renders the seed germination process insensitive to combined JA, auxin, and ABA. Collectively, our findings unveil the MYC–ARF10/ARF16–ABI5 module as a pivotal molecular switch that integrates JA, auxin, and ABA signaling pathways, thereby enabling plants to mount adaptive responses to challenging environmental conditions.