Honors & Awards

  • Dean’s Postdoctoral Fellowship, Stanford School of Medicine (2024)
  • Kavli-Helinski Endowed Graduate Fellowship, School of Biological Sciences, UC San Diego (2020)
  • Innovative Research Grant, The Kavli Institute for Brain and Mind (2020)
  • National Scholarship, Chinese Ministry of Education (2014)

Professional Education

  • Doctor of Philosophy, University of California San Diego (2023)

Stanford Advisors

All Publications

  • An intraflagellar transport dependent negative feedback regulates the MAPKKK DLK-1 to protect cilia from degeneration. Proceedings of the National Academy of Sciences of the United States of America Sun, Y., Jin, Y. 2023; 120 (39): e2302801120


    Primary cilia are specialized organelles supporting the development and function of cells and organisms. Intraflagellar transport (IFT) is essential for cilia formation, maintenance, and function. In C. elegans ciliated sensory neurons, IFT interacts with signaling molecules to generate distinct morphological and function features and also to maintain the integrity of cilia. Here, we report an IFT-dependent feedback control on the conserved MAPKKK DLK-1 in the ciliated sensory neurons. DLK proteins are widely known to act in synapse formation, axon regeneration, and degeneration, but their roles in other neuronal compartments are understudied. By forward genetic screening for altered expression of the endogenously tagged DLK-1 we identified multiple ift mutants showing increased DLK-1 accumulation in the defective sensory endings. We show that in response to acute IFT disruption, DLK-1 accumulates rapidly and reversibly. The expression levels of the transcription factor CEBP-1, known to act downstream of DLK-1 in the development and maintenance of synapses and axons, are also increased in the ciliated sensory neurons of ift mutants. Interestingly, the regulation of CEBP-1 expression shows sensory neuron-type dependency on DLK-1. Moreover, in the sensory neuron AWC, which has elaborate cilia morphology, up-regulated CEBP-1 represses DLK-1 at the transcription level, thereby dampening DLK-1 accumulation. Last, the IFT-dependent regulatory loop of DLK-1 and CEBP-1 offers neuroprotection in a cilia degeneration model. These findings uncover a surveillance mechanism in which tight control on the DLK-1 signaling protects cilia integrity in a context-specific manner.

    View details for DOI 10.1073/pnas.2302801120

    View details for PubMedID 37722038

    View details for PubMedCentralID PMC10523469

  • Coupled Control of Distal Axon Integrity and Somal Responses to Axonal Damage by the Palmitoyl Acyltransferase ZDHHC17. Cell reports Niu, J., Sanders, S. S., Jeong, H., Holland, S. M., Sun, Y., Collura, K. M., Hernandez, L. M., Huang, H., Hayden, M. R., Smith, G. M., Hu, Y., Jin, Y., Thomas, G. M. 2020; 33 (7): 108365


    After optic nerve crush (ONC), the cell bodies and distal axons of most retinal ganglion cells (RGCs) degenerate. RGC somal and distal axon degenerations were previously thought to be controlled by two parallel pathways, involving activation of the kinase dual leucine-zipper kinase (DLK) and loss of the axon survival factor nicotinamide mononucleotide adenylyltransferase-2 (NMNAT2), respectively. Here, we report that palmitoylation of both DLK and NMNAT2 by the palmitoyl acyltransferase ZDHHC17 couples these signals. ZDHHC17-dependent palmitoylation enables DLK-dependent somal degeneration after ONC and also ensures NMNAT-dependent distal axon integrity in healthy optic nerves. We provide evidence that ZDHHC17 also controls survival-versus-degeneration decisions in dorsal root ganglion (DRG) neurons, and we identify conserved motifs in NMNAT2 and DLK that govern their ZDHHC17-dependent regulation. These findings suggest that the control of somal and distal axon integrity should be considered as a single, holistic process, mediated by the concerted action of two palmitoylation-dependent pathways.

    View details for DOI 10.1016/j.celrep.2020.108365

    View details for PubMedID 33207199