Yishi Jin
· Distinguished ProfessorVerifiedUniversity of California, San Diego · Neurobiology
Active 1988–2025
About
Yishi Jin is a Distinguished Professor of Neurobiology and the Principal Investigator of the Jin Lab. She received her B.S. degree from Peking University, China, and her Ph.D. from the University of California, Berkeley. Following her doctoral studies, she completed postdoctoral training at the Massachusetts Institute of Technology (MIT). The information provided does not include specific details about her research focus or key contributions.
Research topics
- Cell biology
- Biology
- Computer Science
- Chemistry
- Neuroscience
- Biochemistry
- Internal medicine
- Anatomy
- Composite material
- Genetics
- Biophysics
- Endocrinology
- Telecommunications
- Materials science
Selected publications
2025-02-06
peer-reviewOpen accessSenior authorThe conserved MAP3K12/Dual Leucine Zipper Kinase (DLK) plays versatile roles in neuronal development, axon injury and stress responses, and neurodegeneration, depending on cell-type and cellular contexts. Emerging evidence implicates abnormal DLK signaling in several neurodegenerative diseases. However, our understanding of the DLK-dependent gene network in the central nervous system remains limited. Here, we investigated the roles of DLK in hippocampal glutamatergic neurons using conditional knockout and induced overexpression mice. We found that dorsal CA1 and dentate gyrus neurons are vulnerable to elevated expression of DLK, while CA3 neurons appear less vulnerable. We identified the DLK-dependent translatome that includes conserved molecular signatures and displays cell-type specificity. Increasing DLK signaling is associated with disruptions to microtubules, potentially involving STMN4. Additionally, primary cultured hippocampal neurons expressing different levels of DLK show altered neurite outgrowth, axon specification, and synapse formation. The identification of translational targets of DLK in hippocampal glutamatergic neurons has relevance to our understanding of selective neuron vulnerability under stress and pathological conditions.
eLife · 2025-02-06
preprintOpen accessSenior authorAbstract The conserved MAP3K12/Dual Leucine Zipper Kinase (DLK) plays versatile roles in neuronal development, axon injury and stress responses, and neurodegeneration, depending on cell-type and cellular contexts. Emerging evidence implicates abnormal DLK signaling in several neurodegenerative diseases. However, our understanding of the DLK-dependent gene network in the central nervous system remains limited. Here, we investigated the roles of DLK in hippocampal glutamatergic neurons using conditional knockout and induced overexpression mice. We found that dorsal CA1 and dentate gyrus neurons are vulnerable to elevated expression of DLK, while CA3 neurons appear less vulnerable. We identified the DLK-dependent translatome that includes conserved molecular signatures and displays cell-type specificity. Increasing DLK signaling is associated with disruptions to microtubules, potentially involving STMN4. Additionally, primary cultured hippocampal neurons expressing different levels of DLK show altered neurite outgrowth, axon specification, and synapse formation. The identification of translational targets of DLK in hippocampal glutamatergic neurons has relevance to our understanding of selective neuron vulnerability under stress and pathological conditions.
eLife · 2025-03-11
articleOpen accessSenior authorThe conserved MAP3K12/Dual Leucine Zipper Kinase (DLK) plays versatile roles in neuronal development, axon injury and stress responses, and neurodegeneration, depending on cell-type and cellular contexts. Emerging evidence implicates abnormal DLK signaling in several neurodegenerative diseases. However, our understanding of the DLK-dependent gene network in the central nervous system remains limited. Here, we investigated the roles of DLK in hippocampal glutamatergic neurons using conditional knockout and induced overexpression mice. We found that dorsal CA1 and dentate gyrus neurons are vulnerable to elevated expression of DLK, while CA3 neurons appear less vulnerable. We identified the DLK-dependent translatome that includes conserved molecular signatures and displays cell-type specificity. Increasing DLK signaling is associated with disruptions to microtubules, potentially involving STMN4. Additionally, primary cultured hippocampal neurons expressing different levels of DLK show altered neurite outgrowth, axon specification, and synapse formation. The identification of translational targets of DLK in hippocampal glutamatergic neurons has relevance to our understanding of selective neuron vulnerability under stress and pathological conditions.
Annual Review of Genetics · 2025-11-25 · 2 citations
articleOpen accessSenior authorThe MAP3K dual-leucine zipper kinases are stress-sensing signaling molecules that have important roles in neuronal development and maintenance, traumatic injury, and neurodegeneration. These kinases activate signal transduction cascades and elicit distinct cellular phenotypes in response to a variety of physiological and pathological stimuli. Studies from animal and cellular models have supported their conserved functions and also highlight context and cell-type specificity. This review focuses on recent findings on the molecular landscape associated with these kinases and discusses key themes of the DLK function network in the mammalian nervous system.
A tubulin–MAPKKK pathway engages tubulin isotype interaction for neuroprotection
Proceedings of the National Academy of Sciences · 2025-08-14 · 1 citations
articleOpen accessSenior authorThe microtubule (MT) cytoskeleton is essential for neuronal morphology, neurite growth, synapse formation and maintenance, as well as regulation of signal transduction. Most cells express multiple isotypes of α- and β-tubulin that can coassemble into MTs. While a variety of signaling pathways regulate MT integrity and homeostasis, little is known about how tubulin isotypes interact in vivo. Here, we report a mechanism in which altered function of a neuronal β-tubulin in Caenorhabditis elegans activates the conserved kinase DLK-1 and its downstream signal transduction, which in turn upregulates expression of an α-tubulin isotype to ensure MT integrity. We find that alteration in the T7 loop of the β-tubulin/BEN-1 causes the formation of BEN-1-enriched islands along MTs in neurites. Combining genome editing with cellular imaging, we identified amino acid residues in α-tubulin/TBA-2 that are necessary for formation of BEN-1 islands. Activation of DLK-1 signaling in ben-1 mutants promotes TBA-2 transcription and protects axon and synapse morphology. These data uncover a positive feedback loop between DLK-1 and regulation of tubulin isotype interaction that maintains neuronal resilience.
2025-03-11
peer-reviewOpen accessSenior authorDLK signaling network reveals the conserved function in neuritogenesis and synapse formation, and highlights the regulation of c-Jun translation and microtubule homeostasis in hippocampal selective neuron vulnerability.
G3 Genes Genomes Genetics · 2025-01-24 · 1 citations
articleOpen accessSenior authorThe conserved MAP3K DLKs are widely known for their functions in synapse formation, axonal regeneration and degeneration, and neuronal survival, notably under traumatic injury and chronic disease conditions. In contrast, their roles in other neuronal compartments are much less explored. Through an unbiased forward genetic screening in C. elegans for altered patterns of GFP-tagged DLK-1 expressed from the endogenous locus, we have recently uncovered a mechanism by which the abundance of DLK-1 is tightly regulated by intraflagellar transport in ciliated sensory neurons. Here, we report additional mutants identified from the genetic screen. Most mutants exhibit increased accumulation of GFP::DLK-1 in sensory endings, and the levels of misaccumulated GFP::DLK-1 are exacerbated by loss of function in cebp-1, the b-Zip transcription factor acting downstream of DLK-1. We identify several new mutations in genes encoding proteins functioning in intraflagellar transport and cilia assembly, in components of BBSome, MAPK-15, and DYF-5 kinases. We report a novel mutation in the chaperone HSP90 that causes misaccumulation of GFP::DLK-1 and up-regulation of CEBP-1 selectively in ciliated sensory neurons. We also find that the guanylate cyclase ODR-1 constrains GFP::DLK-1 abundance throughout cilia and dendrites of AWC neurons. Moreover, in odr-1 mutants, AWC cilia display distorted morphology, which is ameliorated by loss of function in dlk-1 or cebp-1. These data expand the landscape of DLK-1 signaling in ciliated sensory neurons and underscore a high degree of cell- and neurite- specific regulation.
Phospholipid biogenesis maintains neuronal integrity during aging and axon regeneration
Genetics · 2025-06-25 · 1 citations
articleOpen accessNeurons maintain their morphology over prolonged periods of adult life with limited regenerative capacity. Among the various factors that shape neuronal morphology, lipids function as membrane components, signaling molecules, and regulators of synaptic plasticity. Here, we tested genes involved in phospholipid biosynthesis and identified their roles in axon regrowth and maintenance. CEPT-2 and EPT-1 are enzymes catalyzing the final steps in the de novo phospholipid synthesis (Kennedy) pathway. Loss of function mutants of cept-2 or ept-1 show reduced axon regrowth and failure to maintain axon morphology. We demonstrate that CEPT-2 is required cell-autonomously to prevent age-related axonal morphology defects. We further investigated genetic interactions of cept-2 or ept-1 with dip-2, a conserved regulator of lipid metabolism that affects axon morphology maintenance and regrowth after injury. Loss-of-function in dip-2 led to suppression of axon regrowth defects observed in either cept-2 or ept-2 mutants, suggesting that DIP-2 acts to counterbalance phospholipid synthesis. Our findings reveal the genetic regulation of lipid metabolism as critical for axon maintenance following injury and during aging.
bioRxiv (Cold Spring Harbor Laboratory) · 2025-02-08
preprintOpen accessAbstract Neurons maintain their morphology over prolonged periods of adult life with limited regeneration after injury. C. elegans DIP-2 is a conserved regulator of lipid metabolism that affects axon maintenance and regeneration after injury. Here, we investigated genetic interactions of dip-2 with mutants in genes involved in lipid biosynthesis and identified roles of phospholipids in axon regrowth and maintenance. CEPT-2 and EPT-1 are enzymes catalyzing the final steps in the de novo phospholipid synthesis (Kennedy) pathway. Loss of function mutants of cept-2 or ept-1 show reduced axon regrowth and failure to maintain axon morphology. We demonstrate that CEPT-2 is cell-autonomously required to prevent age-related axonal defects. Interestingly, loss of function in dip-2 led to suppression of the axon regrowth phenotype observed in either cept-2 or ept-2 mutants, suggesting that DIP-2 acts to counterbalance phospholipid synthesis. Our findings reveal the genetic regulation of lipid metabolism to be critical for axon maintenance under injury and during aging. Article Summary Little is known about how adult neurons live long with limited regenerative capacity. This study investigates the role of lipid metabolism in sustaining neuronal health in C. elegans. Mutating phospholipid synthetic genes impairs axon regrowth after injury. Lack of DIP-2, a lipid regulator, restores regrowth, suggesting DIP-2 counterbalances phospholipid synthesis. Moreover, neuronal phospholipid synthesis is essential for preventing age-dependent axonal defects. These findings reveal phospholipid biosynthesis is key to axon integrity during aging and injury. As lipid metabolism is implicated in neurological disorders, this study serves as an entry point into investigating neuronal lipid biology under various conditions.
The BEN domain protein LIN-14 coordinates neuromuscular positioning during epidermal maturation
iScience · 2024-12-12
articleOpen accessSenior authormutants show defects in formation of epidermis-muscle attachment complex hemidesmosomes in the maturing ventral epidermis, leading to detachment of muscles and motor neurons as well as movement defects. Our findings reveal a cell non-autonomous role for LIN-14 in coordinating inter-tissue interaction and neuromuscular positioning during epidermal maturation.
Recent grants
Neural Circuits Postdoctoral Training Program
NIH · $6.0M · 1982–2024
Cellular Dynamics of Axon Regeneration
NIH · $3.7M · 2015–2024
NIH · $388k · 2016
CAREER: Synaptic Remodeling in C. elegans
NSF · $500k · 1999–2005
GABAergic Neuron Differentiation in C.elegans
NIH · $2.4M · 1996–2022
Frequent coauthors
- 78 shared
Alexandr Goncharov
University of California, San Diego
- 72 shared
Andrew Chisholm
University of California, San Diego
- 48 shared
Yingchuan Qi
- 40 shared
Zilu Wu
University of California, San Diego
- 36 shared
Dong Yan
Army Medical University
- 35 shared
Mei Zhen
Mount Sinai Hospital
- 33 shared
H. Robert Horvitz
McGovern Institute for Brain Research
- 31 shared
Roger Y. Tsien
Howard Hughes Medical Institute
Labs
Jin LabPI
Not provided
Education
- 1991
PhD, Molecular Biology
University of California Berkeley
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