CIMR-Yinwen Liang

Research Group

Yinwen Liang

liangyinwen(at)cimrbj.ac.cn

Assistant Investigator

liangyinwen(at)cimrbj.ac.cn

B.S. in Biology, Xiamen University, Xiamen, China

Ph.D. in Cellular and Developmental Biology, Tsinghua University, Beijing, China

Work Experience

2026.1-Present

Assistant investigator, Chinese Institutes for Medical Research, Beijing, China

2021.2-2025.9

Senior Research Scientist, Memorial Sloan Kettering Cancer Center, New York, USA

2016.6-2021.1

Research Fellow, Memorial Sloan Kettering Cancer Center, New York, USA

2014.7-2016.6

Research Associate, Tsinghua University, Beijing, China

Research Direction

The Liang laboratory at CIMR works on understanding mammalian development and tissues hemostasis, with a particular emphasis on the vital organelle, cilium. Cilia are present on the surface of most cells, play critical roles in motility, sensing, and signaling transduction, particularly Hedgehog (Hh) signaling pathway. Using genetic and multi-omics approaches, the Liang laboratory aims to uncover the molecular mechanism behind cilia formation and dysfunction, specifically in ciliopathies and Hedgehog signaling-related brain tumors (SHH-medulloblastoma). The laboratory is committed to advancing the understanding of these mechanisms to develop therapeutic strategies for treating related diseases.

Primary cilia (red) on the surface of cells. Defects in these antenna-like structures can cause a variety of diseases, called ciliopathies.

HH signaling is essential for embryonic development and tissue homeostasis, while overaction of HH signaling results in tumor formation. Left, wildtype and Shh null mouse embryos; Right, MRI images of SHH-medulloblastoma.

Major Research Projects

1. Identifying novel regulators of the ciliary gene regulatory network

The lab has identified two key transcription factors SP5/8 of SP/KLF family binds to GC box of numerous ciliary genes, but how these TFs specially activating ciliary genes remains unclear. We hypothesize that cofactors, inductive signals and lineage-specific TFs play significant roles. Through forward genetic screens, the team have discovered novel regulators that mediate mRNA stability of cilia genes (publication in preparation). We are currently employing perturb-seq combined with high-throughput CRISPR screens to elucidate the detailed gene regulatory network involved in cilia formation.

2. Dissecting cell-type-specific cilia formation and morphological diversity

The laboratory is exploring how different cell types regulate cilia formation and maintain the diversity of cilia morphology, which is essential for proper cellular function and tissue homeostasis.

3. Understanding the molecular mechanisms of ciliopathiesand SHH-medulloblastoma

Building on earlier discoveries, the lab is investigating the roles of SP/KLF family transcription factors and newly identified regulators in ciliopathies and SHH-medulloblastoma using induced pluripotent stem cell (iPSC)-derived airway organoids. The long-term goal is to harness the regulation of cilia formation as a therapeutic strategy to treat ciliopathies and Hedgehog-driven tumors.

4. Exploring the roles of primary cilia in neuron maturation and differentiation

The Liang laboratory is studying the critical role of primary cilia in the maturation and differentiation of neurons and aiming to use insights from the gene regulatory network to rejuvenate the brain following injury or aging.

Major Contributions

1. Discovered transcription factors SP5 and SP8 as key transcriptional regulators in cilia formation (Science, 2025)

The laboratory discovered SP5 and SP8 as key transcriptional regulators of cilia formation, demonstrated that SP5 and SP8 directly bind to and activate numerous cilia gene expression, including Foxj1 and RFX family TFs genes. Ectopic expression of SP8 can induce cilia formation in naturally unciliated cells, these two TFs are both necessary and sufficient to drive cilia formation (Science, 2025).

2. Uncovered the mechanisms of intraflagellar transport machinery and cilia assembly (Current Biology, 2018; Developmental Cell, 2014a; Developmental Cell, 2014b)

The Liang lab uncovered the molecular mechanisms governing intraflagellar transport (IFT) and cilia assembly, including the regulation of motor protein KIF3B via phosphorylation at S663. We also discovered a cilia-length regulation model through the regulation of IFT loading rate. (Current Biology, 2018; Developmental Cell, 2014a; Developmental Cell, 2014b)

3. Revealed molecular insights into ciliopathies and SHH-medulloblastoma (Science, 2025; eLife, 2025; Journal of Cell Biology, 2018; American Journal of Human Genetics, 2018)

Representative Publications *：Co-first author; #：Co-corresponding author

Liang Y^#, Koche R, Chalamalasetty RB, Stephen DN, Kennedy MW, Lao Z, Pang Y, Kuo YY, Lee M, Lobo FP, Huang X, Hadjantonakis AK, Yamaguchi TP, Anderson KV, Joyner AL^#. Transcription factors SP5 and SP8 drive primary cilia formation in mammalian embryos. Science, 2025, 389 (6763): eadt5663. DOI: 10.1126/science. adt5663

Lao Z, Nagar SE, Liang Y, Stephen DN, Joyner AL. PTEN restrains SHH medulloblastma growth through cell autonomous and nonautonomous mechanisms. eLife, 2025. DOI: 10.1101/2025.07.31.667996

Liang Y, Zhu X, Wu Q, Pan J. Ciliary Length Sensing Regulates IFT Entry via Changes in FLA8/KIF3B Phosphorylation to Control Ciliary Assembly. Current Biology, 2018, 28(15): 2429-2435.e3. DOI: 10.1016/j.cub.2018.05.069

Agbu SO*, Liang Y*, Liu A, Anderson KV. The small GTPase RSG1 controls a final step in primary cilia initiation. Journal of Cell Biology, 2018, 217(1): 413-427. DOI: 10.1083/jcb.201604048

Liang Y*, Pang Y*, Wu Q, Hu Z, Han X, Xu Y, Deng H, Pan J. FLA8/KIF3B phosphorylation regulates kinesin-II interaction with IFT-B to control IFT entry and turnaround. Developmental Cell, 2014, 30(5): 585-97. DOI: 10.1016/j.devcel.2014.07.019 (Highlighted by Craige B and Witman G. Flipping a Phosphate Switch on Kinesin-II to Turn IFT Around. Developmental Cell, 2014, DOI: 10.1016/j.devcel.2014.08.019)

Liang Y, Meng D, Zhu B, Pan J. Mechanism of ciliary disassembly. Cellular and Molecular Life Sciences, 2016, 73(9): 1787-802. DOI: 10.1007/s00018-016-2148-7

Liang Y, Pan J. Regulation of flagellar biogenesis by a calcium dependent protein kinase in Chlamydomonas reinhardtii. PLoS One, 2013, 8(7): e69902. DOI: 10.1371/journal.pone.0069902

Eguether T, San Agustin JT, Keady BT, Jonassen JA, Liang Y, Francis R, Tobita K, Johnson CA, Abdelhamed ZA, Lo CW, Pazour GJ. IFT27 links the BBSome to IFT for maintenance of the ciliary signaling compartment. Developmental Cell, 2014, 31(3): 279-290. DOI: 10.1016/j.devcel.2014.09.011

Full List of Publications Can Be Found: here