China Education Equipment Purchasing Network News: According to Beijing Yanji Bioreagent Co., Ltd., Luo Zhenge's research group from the Institute of Neuroscience, Shanghai Academy of Life Sciences, Chinese Academy of Sciences mainly studies the molecular mechanism of neuronal morphogenesis and synapse formation, focusing on neuronal polarity Establish mechanisms and regulate intracellular and extracellular signaling mechanisms of axon dendritic differentiation (PNAS, 2006, 2008; Nature Cell Biology, 2007; JBC, 2011; Developmental Cell, 2011); In addition, use neuromuscular junctions as models to study synaptic differentiation and The molecular mechanism of remodeling (Neuron, 2002, 2003, 2007; JBC, 2008; J. Neurosci. 2010). In 2011, this research group published JBC, Developmental Cell magazine one after another, and made important research progress. In addition, this research group is currently recruiting post-doctoral fellows, assistant researchers and research assistants, and interested readers can follow.
In the latest "Developmental Cell" article, members of this research team discovered the asymmetric insertion mechanism of cell membranes during the development of neuronal axons, and made new progress in the research of neuron polarization and axon development.
Neurons have a typical polar structure, complex branch dendrites are responsible for receiving information, and a single axon is responsible for outputting information. The differentiation of a neurite of a new neuron into an axon is called the polarization of the neuron. This process requires a rapid increase of the cell membrane towards the neurite. Its regulation mechanism is an important unresolved scientific issue.
Under the guidance of researcher Luo Zhenge, doctoral students Wang Tong and Liu Yang conducted in-depth research on this issue. They found that the tumor suppressor protein Lgl1 plays an important role in this process. Lgl1 is located on the cytoplasmic side of plasmalemmal precursor vesicle (PPV) and has a polar distribution during axon development. In cultured hippocampal neurons, down-regulation of Lgl1 inhibits the insertion of PPV into the cell membrane and depolarizes the neurons. Overexpression of Lgl1 promotes axon development. Further mechanism research shows that Lgl1 works by regulating the small G protein Rab10. Lgl1 can dissociate Rab10 from GDI (GDP-dissociation inhibitor) in the cytoplasm, thereby promoting the localization of Rab10 to PPV. Down-regulating the expression of Rab10 or inhibiting its activity will also affect the membrane insertion of PPV, making neurons lose polarity, and up-regulating its expression will promote axon development. Lgl1 regulates the insertion of PPV into the cell membrane and the polarization of neurons through Rab10. Subsequent work is deeply studying the transport mechanism, effector factors, membrane localization and membrane fusion signals of Rab10 vesicles.
Another article focuses on another research direction: using hippocampal neurons cultured in vitro as a model to select molecules that determine or affect the polarity of neurons, especially those that regulate the microtubule and actin cytoskeletal organization.
The researchers discovered a new role of the Wnt / Ca2 + signaling pathway in the regulation of actin and growth cone dynamics, and thus analyzed the mechanism of cytoskeletal remodeling mediated by extracellular factors. This provides new clues for a deeper understanding of the structural mechanism of the actin cytoskeleton organization structure.
(Biometrics: Wan Wen)
Original summary:
Lgl1 Activation of Rab10 Promotes Axonal Membrane Trafficking Underlying Neuronal Polarization
Directed membrane trafficking is believed to be crucial for axon development during neuronal morphogenesis. However, the underlying mechanisms are poorly understood. Here, we report a role of Lgl1, the mammalian homolog of Drosophila tumor suppressor Lethal giant larvae, in controlling membrane trafficking underlying axonal growth. We find that Lgl1 is associated with plasmalemmal precursor vesicles and enriched in developing axons. Lgl1 upregulation promoted axonal growth, whereas downregulation attenuated it as well as directional membrane insertion. Interestingly, Lgl1 interacted with and activated Rab10, a small GTPase that mediates membrane protein trafficking, by releasing GDP dissociation inhibitor (GDI) from Rab10. Furthermore, Rab10 lies downstream of Lgl1 in axon development and directional membrane insertion. Finally, both Lgl1 and Rab10 are required for neocortical neuronal polarization in vivo. Thus, the Lgl1 regulation of Rab10 stimulates the trafficking of membrane precu rsor vesicles, whose fusion with the plasmalemma is crucial for axonal growth.
Calpain activation by Wingless-type murine mammary tumor virus integration site family, member 5A (Wnt5a) promotes axonal growth.
Axon development involves spatial-temporal cytoskeletal reorganization. However, how the cytoskeleton remodeling is modulated by extracellular cues is unclear. Here, we report a role of Wnt / Ca2 + signaling in regulating actin and growth cone dynamics. We found that treatment of cultured cortical neurons with Wnt5a, a non-canonical Wnt, either globally or locally, caused an increase in the activity of calpain, a calcium-dependent protease responsible for the cleavage of several actin binding proteins, including spectrin. Treatment with Wnt5a promoted growth cone advance, as well as axonal growth, and these effects were prevented by chelating intracellular calcium, inhibition or down-regulation of calpain, or blockade of spectrin cleavage by competitive peptides. Interestingly, both Wnt5a and activated calpain were found to be mainly distributed in the axon-rich intermediate zone of neocortex. Down-regulating calpain expression interfered with the growth of callosal axons in vivo. Thus, W nt5a serves as a physiological cue to stimulate localized calpain activity, which in turn promotes growth cone advance and axonal growth.
About the Author:
Luo Zhenge
Born in January 1967, researcher and assistant director of the Institute of Neuroscience, Shanghai Academy of Life Sciences, Chinese Academy of Sciences.
1984-1988, Department of Biology, Nankai University, Bachelor 1988-1991, Academy of Military Medical Sciences, Master 1991-1992, Department of Infectious Diseases, Tianjin 254 Hospital, Physician 1992-1995, Doctor of Military Medical Sciences 1995-1999, Military Medicine Assistant Researcher and Associate Researcher of the Immunology Laboratory of the Institute of Microbiology and Epidemiology, Academy of Sciences, and serves as the Executive Deputy Director of the Laboratory. 2000.01-2003. 05, Postdoctor, Department of Neurobiology, University of Alabama at Birmingham (UAB). 2003.06-present, researcher and doctoral supervisor of Shanghai Institute of Life Sciences, Chinese Academy of Sciences.
research direction:
Dr. Luo Zhenge is mainly engaged in the research of molecular and cellular mechanism of neural development, especially the molecular mechanism of neuronal morphogenesis and the mechanism of synapse formation and remodeling. A series of research achievements have been made in the important areas of neurodevelopment such as neuronal polarity establishment, neuronal axis-dendritic development and synapse formation. Published a series of research papers in international academic journals including "Nature Cell Biology" and "Neuron", and has been cited 433 times by others. It has trained 17 master and doctoral students. Dr. Luo Zhenge was selected by the Academy of Sciences' "Hundred Talents Program". The final evaluation was excellent; he was supported by the "National Outstanding Youth Fund" and served as the head of the innovative research group of the National Natural Science Foundation of China. He has won honorary titles such as "China Youth Science and Technology Award", "National Candidate for the New Century Talent Project" and "Shanghai Academic Leader".
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