Heng Li
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Heng Li has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Chunmei Niu
Laboratory for Animal Behavioral Physiology, College of Bioscience and Biotechnology, Yangzhou University, Yangzhou, China
1 shared publication - Churui Ge
Laboratory for Animal Behavioral Physiology, College of Bioscience and Biotechnology, Yangzhou University, Yangzhou, China
1 shared publication - Peng Wang
Laboratory for Animal Behavioral Physiology, College of Bioscience and Biotechnology, Yangzhou University, Yangzhou, China
1 shared publication - Shuang Liu
Laboratory for Animal Behavioral Physiology, College of Bioscience and Biotechnology, Yangzhou University, Yangzhou, China
1 shared publication - Weikang Fan
Laboratory for Animal Behavioral Physiology, College of Bioscience and Biotechnology, Yangzhou University, Yangzhou, China
1 shared publication - Yang Cheng
State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
1 shared publication
Latest Publications
- 13 July 2026
- Published by Rockefeller University Press in Journal of Cell Biology
- Vol. 225 (9)
Rag GTPases and mTORC1 regulate intestinal stem cell activity in response to nutrient availability.
The intestinal epithelium, predominantly composed of enterocytes (ECs), integrates dietary cues to regulate intestinal stem cell (ISC) activity and maintain intestinal homeostasis. However, the underlying mechanisms remain incompletely understood. Here, we demonstrate the functions of essential nutrient-sensing mediators Rag GTPases and mTORC1 on Drosophila ISC activity. Inhibition of Rag GTPases in ECs triggers Mitf activation, which subsequently induces Upd3 expression to non-cell autonomously increase the ISC proliferation and differentiation through stimulating the JAK-STAT pathway. Inactivation of mTORC1 in ECs also activates the Upd3-JAK-STAT axis and increases ISC activity, but through a Mitf-independent mechanism. Moreover, in contrast to mTORC1 inactivation blocking ISC proliferation and differentiation, depletion of Rag GTPases in ISCs shows no obvious cell autonomous effect on ISC activity. Consistent with inhibition of the nutrient-responsive pathway in ECs promoting ISC proliferation, long-term nutrient starvation enhances ISC activity and Upd3 expression. Together, our findings reveal a nutrient-sensing regulatory network that controls ISC proliferation involving the Rag GTPases-Mitf axis and mTORC1 activity.
- 13 July 2026
- Published by Rockefeller University Press in Journal of Cell Biology
- Vol. 225 (9)
Rag GTPases and mTORC1 regulate intestinal stem cell activity in response to nutrient availability.
The intestinal epithelium, predominantly composed of enterocytes (ECs), integrates dietary cues to regulate intestinal stem cell (ISC) activity and maintain intestinal homeostasis. However, the underlying mechanisms remain incompletely understood. Here, we demonstrate the functions of essential nutrient-sensing mediators Rag GTPases and mTORC1 on Drosophila ISC activity. Inhibition of Rag GTPases in ECs triggers Mitf activation, which subsequently induces Upd3 expression to non-cell autonomously increase the ISC proliferation and differentiation through stimulating the JAK-STAT pathway. Inactivation of mTORC1 in ECs also activates the Upd3-JAK-STAT axis and increases ISC activity, but through a Mitf-independent mechanism. Moreover, in contrast to mTORC1 inactivation blocking ISC proliferation and differentiation, depletion of Rag GTPases in ISCs shows no obvious cell autonomous effect on ISC activity. Consistent with inhibition of the nutrient-responsive pathway in ECs promoting ISC proliferation, long-term nutrient starvation enhances ISC activity and Upd3 expression. Together, our findings reveal a nutrient-sensing regulatory network that controls ISC proliferation involving the Rag GTPases-Mitf axis and mTORC1 activity.