Baojin Ding, PhD
Assistant Professor of Biochemistry and Molecular Biology
Bachelor of Science - 2001 (Medicine, MD equivalent), Medical College of Qingdao University, China
Master of Science - 2004 (Clinical Laboratory), Wenzhou Medical University, China
PhD - 2010 (Biochemistry and Molecular Biology), Louisiana State University, Baton Rouge, LA
DING LAB NEWS
May 6, 2022
Paper from the Ding Lab published in the journal Stem Cell Research. This is a Lab Resource paper. In this study, the disease-causing mutation in a dystonia patient iPSC line was genomically corrected and generated isogenic iPSC control lines, providing valuable research recourses in dystonia research.
Akter M, Cui H, Chen YH and Ding B*. (2022). Generation of gene-corrected isogenic control cell lines from a DYT1 dystonia patient iPSC line carrying a heterozygous GAG mutation in TOR1A gene. Stem Cell Research. 62. 102807
May 2, 2022
Congratulations on Dr. Masood Sepehrimanesh joining the Ding Lab as a Postdoctoral Fellow. Welcome Masood!
March 18, 2022
Paper from the Ding Lab published in the journal STAR Protocols (Cell Press). This paper is an invited protocol for the generation of patient-specific motor neurons from hiPSCs.
Akter M, Cui H, Sepehrimanesh M., Hosain A. and Ding B*. (2022). Generation of highly pure motor neurons from human induced pluripotent stem cells. STAR Protoc. 2022 Mar 10; 3(1):101223.doi: 10.1016/j.xpro.2022.101223. eCollection 2022 Mar 18
January 29, 2022
Congratulations to the Ding Lab for the publication (Ding et al. Disease modeling with human neurons reveals LMNB1 dysregulation underlying DYT1 dystonia. J Neurosci. (2021) 41 (9): 2024-2038.) was selected as JNeurosci Spotlight 2021.
JNeurosci's Annual Spotlight features articles that received the highest marks for both methodological merit and significance. See the papers selected for this year’s recognition.
January 27, 2022
Research Features: Patient-specific neurons key in new dystonia discoveries
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February 12, 2020
Congratulations to the Ding Lab on receiving a grant from the National Institutes of Health (NIH). This is the National Institute of Neurological Disorders and Stroke (NINDS) Exploratory Neuroscience Research Grant. The project aims to determine the pathogenesis of childhood-onset DYT1 dystonia in patient-specific neurons that are generated by direct conversion and iPSC-based reprogramming and differentiation.
November 15, 2019
Congratulations to the Ding Lab on receiving a grant from the Department of Defense (DoD) Peer-Reviewed Medical Research Program (PRMRP) Discovery Award. This project aims to determine the pathogenesis of adulthood onset dystonia via directly reprogramming human neurons from patient fibroblasts.
Our research focuses on cellular and molecular neuroscience and neurological diseases. Cell culture and genetically modified mice are used as model systems. Techniques in Molecular Biology, Cell Biology and Biochemistry are employed.
Our research projects can be grouped into three closely correlated directions.
- 1. The timing mechanism of gene expression in maturing neurons
- 2. Nucleocytoplasmic transport regulation
- 3. Modeling human neurological diseases
The timing mechanism of gene expression in maturing neurons
Central nervous system development results from the interactions between intrinsic genes and extrinsic environment. The process of neuronal development consists of successive developmental stages including proliferation, differentiation, migration, ax on extension, dendritogenesis, and formation of functional synapses. In this developmental sequence, the interplay between genes and environment ensures that each step must occur in the proper timing and sequence. Their successful regulation requires that numerous groups of genes be turned on and off in a timely manner. However, the timing mechanisms of gene expression in maturing neurons are not fully understood.
By using mouse cerebellar granule neurons (CGNs) as a research model, we have identified a novel nuclear factor one (NFI)-regulated temporal switch program linked to dendrite formation. In this program, neuronal mature genes (late expressed synaptoge nesis-related genes) are up-regulated and immature genes (early expressed amplification-related genes) are down-regulated during a period of postnatal development window. One distinguished feature of this program is the NFI temporal occupancy of target genes. We also found that NFI switch program were regulated by resting membrane potential, CaN/NFAT signaling pathway, ETV1 and BDNF etc. Most interestingly, some neurodevelopmental disorders are associated with particular NFI-regulated 'switch' genes, such as Autism Spectrum Disorders (ASD). Research efforts are focusing on identification and characterization of novel regulators and signaling pathways of NFI-regulated program, and the involvement of disrupted NFI-regulated developmental program in neurodevelopmental disorders.
Nucleocytoplasmic transport regulation
In eukaryotic cells, transcription and translation processes are physically separated by nuclear envelope (NE). Thus, the proper functions of a cell involves the mRNA nuclear exporting for protein synthesis in the cytoplasm and protein nuclear transport cross the NE (Figure 2A). Defective nucleocytoplasmic transport (NCT) has merged as a common molecular underpinning of many neurological diseases, including Alzheimer disease (AD), amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD). Systematically analyze the regulation of nucleocytoplasmic transport will provide novel insights into the nuclear transport machinery and advance our understanding of how defective NCT contributes to human diseases. We use electron microscope (EM) to examine the ultrastructure of cells, including nuclear envelope and nuclear pore complex (NPC). We have established two systems to analyze nuclear transport function in cultured mammalian cells. One approach measures nuclear mRNA exporting using fluorescent in situ hybridization (FISH) with oligo-dT probes combined with immuno-staining of NE markers. Another approach analyzes protein nuclear transport using lentiviral delivery of a dual reporter (GFP-NES and RFP-NLS). Research efforts are focusing on molecular mechanisms of NCT machinery and identification of dysregulated factors that disrupt NCT in aging and diseased cells.
Modeling human neurological diseases
The limited access to patient neurons greatly impedes the progress of research in neurological diseases. Reprogramming of human neurons from adult fibroblasts provides an unprecedented approach to deciphering the molecular pathogenesis underlying disease condition. Using lentiviral delivery of transcription factors, we can generate human neurons from adult fibroblast via two strategies. One strategy is direct conversion of fibroblasts into neurons. The other strategy is induced pluripotent stem cells (iPSCs)-based reprogramming and differentiation. Research efforts are focusing on the molecular pathogenesis of neurological disorders, such as Alzheimer disease (AD), Dystonia and amyotrophic lateral sclerosis (ALS).
Sepehrimanesh M., Akter M. and Ding B*. (2021). Direct conversion of adult fibroblasts into motor neurons. STAR Protocols. 2 (4) 17 December 2021, 100917 (Cell Press, Invited protocol)
Akter M, Cui H, Chen Y-H and Ding B*. (2021). Generation of two induced pluripotent stem cell lines with heterozygous and homozygous GAG deletion in TOR1A gene from a healthy hiPSC line. Stem Cell Research. 56 (2021)102536 / PDF
Ding B* and Sepehrimanesh M. (2021). Nucleocytoplasmic transport: regulatory mechanisms and the implications in neurodegeneration. Int. J. Mol. Sci. 22 (8): 4165 / PDF
Ding B*, Tang Y, Ma S, Akter M, Liu ML, Zang T, Zhang CL.(2021). Disease modeling with human neurons reveals LMNB1 dysregulation underlying DYT1 dystonia. J Neurosci. 41 (9): 2024-2038. Featured Article, https://www.jneurosci.org/content/41/9/1846
Sepehrimanesh M, and Ding B* (2020). Generation and Optimization of Highly Pure Motor Neurons from Human Induced Pluripotent Stem Cells via Lentiviral Delivery of Transcription Factors. Am J Physiol Cell Physiol. 319: C771–C780.
Ding B,* Akter M, and Zhang C-L. (2020). Differential Influence of Sample Sex and Neuronal Maturation on mRNA and Protein Transport in Induced Human Neurons. Front Mol Neurosci. 2020 Apr 3; 13: 46.
Selvam K, Ding B, Sharma R and Li S. (2019). Evidence that moderate eviction of Spt5 and promotion of error-free transcriptional bypass by Rad26 facilitates transcription coupled repair. J Mol Biol. 2019 Feb 18. doi: 10.1016
Ding B, Dobner PR, Mullikin-Kilpatrick D, Wang W, Zhu H, Chow CW, Gronostajski RM and Kilpatrick DL. (2018). BDNF Activates an NFI-Dependent Neurodevelopmental Timing Program By Sequestering NFATc4. Mol Biol Cell. 2018 Apr 15; 29(8):975-987
Li Y, Hassinger L, Thomson T, Ding B, Ashley J, Hassinger W and Budnik V. (2016). Lamin Mutations Accelerate Aging via Defective Export of Mitochondrial mRNAs through Nuclear Envelope Budding. Curr Biol. 2016 Aug 8;26(15):2052-9
Ding B, Cave HW, Dobner PR, Kilpatrick DM, Bartsokis M, Zhu H, Chow CW, Gronostajski RM and Kilpatrick DL. (2016) Reciprocal Auto-Regulation by NFI Occupancy and ETV1 Promotes the Developmental Expression of Dendrite-Synapse Genes in Cerebellar Granule Neurons. Mol Biol Cell. 2016 May 1;27(9):1488-99
Packard M, Jokhi V, Ding B and Budnik V. (2015) Nucleus to Synapse Nesprin Railroad Tracks Direct Synapse Maturation through RNA localization. Neuron. 86(4):1015-28).
Ding B, Wang W, Selvakumar T, Xi HS, Zhu H, Chow CW, Horton JD, Gronostajski RM and Kilpatrick DL. (2013) Temporal Regulation of Nuclear Factor One Occupancy by Calcineurin/NFAT Governs a Voltage-Sensitive Developmental Switch in Late Maturing Neurons. J Neurosci. 33(7):2860-2872.
Ding B and Kilpatrick DL. (2013) Lentiviral Vector Production, Titration, and Transduction of Primary Neurons. Methods Mol Biol. 1018:119-31. Chapter 12.
Ding B, Lejeune D and Li S. (2010) The C-terminal Repeat Domain of Spt5 Plays an Important Role in Suppression of Rad26-independent Transcription Coupled Repair. J Biol Chem. 285 (8): 5317-5326.
Complete List of my Published Work in MyBibliography: LEARN MORE
We are currently recruiting Post-doctoral Associates. Please contact Dr. Baojin Ding at (firstname.lastname@example.org) for detailed information.
Graduate students interested in conducting research in the Ding lab, please contact Dr. Baojin Ding at (email@example.com) for detailed information.
A position for Undergraduate Student Research Assistant is available in the Ding Lab, please contact Dr. Baojin Ding at (firstname.lastname@example.org) for detailed information.
LSU Health Shreveport
Department of Biochemistry and Molecular Biology
1501 Kings Hwy
Shreveport, LA 71103