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  Location: Home >> Key Laboratories >> State Key Laboratory of Molecular Developmental Biology
State Key Laboratory of Molecular Developmental Biology
The State Key Laboratory of Molecular Developmental Biology is hosted in the Institute of Genetics and Developmental Biology. Our mission is: 1) to address fundamental questions in development of both plants and animals using model organisms such as C. elegans, Drosophila, Xenopus, zebrafish, mouse, monkey, Arabidopsis and rice; and 2) to develop innovative technology to meet national needs in agriculture and human health.
DIRECTOR: Weicai Yang
VICE DIRECTORS: Xun Huang, Jianwu Dai, Fan Chen
PRINCIPAL INVESTIGATORS: Shilai Bao, Yuhang Chen, Zhuo Du, Mei Ding, Weixiang Guo, Yuqiang Jiang, Wei Li, Xiaojiang Li, Jiajia Liu, Runlin Ma, Wenxiang Meng, Guanghou Shui,  Fangzhen Sun, Ye Tian, Qiang Tu, Yingchun
Wang, Zhaohui Wang, Yongbiao Xue, Zhiheng Xu, Chonglin Yang, Jian Zhang, Yongqing Zhang
CHAIR: Zuoyan Zhu
VICE CHAIR: Yongbiao Xue
MEMBERS: Xiang Gao, Aike Guo, Naihe Jing, Jiayang Li, Wei Li, Yixun Liu, Anming Meng, Weihua Wu, Zhihong Xu, Weicai Yang, Xu Zhang
In 2016, the laboratory published 98 papers. Four eminent scientists spoke at the FORUM on DEVELOPMENT, GENETICS, AND DISEASE. During 2016, the laboratory achieved significant advances in the following fields:
Early Development: Weicai Yang’s group reported the identification of a cell-surface receptor heteromer, MDIS1–MIK, on the pollen tube that perceives the female attractant LURE1 in Arabidopsis thaliana. This finding identified the longpuzzled receptor heteromer of the LURE1 attractant and revealed the activation mechanism and will contribute to the full understanding of male-female recognition during plant reproduction. Meanwhile, this study establishes the theory of through inter-species expressing of receptor to break down the reproductive isolation and will shed light in the crop breeding (Wang et al., Nature, 2016). In the Solanaceae, Rosaceae and Plantaginaceae, the S-locus encodes a single S-RNase and a cluster of S-locus F-box (SLF) proteins to control the pistil and pollen expression of SI, respectively. Yongbiao Xue’ s group revealed that the electrostatic potentials act as a major physical force between cytosolic SLFs and S-RNases, providing a mechanistic insight into the self/non-self-discrimination between cytosolic proteins in angiosperms (Li et al., Plant J, 2016). Large numbers of maternal RNAs are deposited in oocytes and are reserved for later development. Jian Zhang’ group reported loss of Zar1 causes markedly upregulation of zona pellucida (ZP) family proteins, while overexpression of ZP proteins in oocytes causes upregulation of stress related activating transcription factor 3 (atf3), arguing that tightly controlled translation of ZP proteins is essential for ER homeostasis during early oogenesis. Furthermore, Zar1 binds to zona pellucida (zp) mRNAs and represses their translation (Miao et al., Development, 2016).
Neurodevelopment and Disease: Zhiheng Xu’s group and Guoli Ming’s group at Johns Hopkins University School of Medicine revealed that Crmp2 (collapsing response mediator protein 2), a schizophrenia risk gene, plays a critical role in neural development, circuit integrity and brain function. They provided a valuable mouse model for better understanding the aetiology of schizophrenia and targeted strategies for drug development (Zhang et al., Nat Commun, 2016). Xu’s group also demonstrated MEA6 plays a critical role in lipid transportation through the coordinated regulation of the COPII machinery, which provided insight into mechanisms underlying VLDL transportation. More importantly, this mouse model provides a useful tool for potential biomarkers or drug screening related to fatty liver disease (Wang et al., Cell Res, 2016). Mei Ding’s group found that the single calponin homology (CH) domain-containing protein CHDP-1 induces the formation of cell protrusions by coupling membrane expansion to Rac1-mediated actin dynamics in C. elegans (Guan et al., PLoS Genet, 2016). Xiaojiang Li’s group revealed age- and cell type-dependent vital functions of Htt (huntingtin, Huntington’s disease protein) and the safety of knocking down neuronal Htt expression in adult brains as a treatment (Wang et al., PNAS, 2016; Liu et al., PLoS Genetics, 2016). The study of Yongqing Zhang’s group shed new light onto the neuronal functions of UBE3A (E3 ubiquitin ligase) and provides novel perspectives for understanding the pathogenesis of UBE3Aassociated Angelman syndrome and autism (Li et al., PLoS Genet, 2016).
Stem Cell and Tissue Engineering: Zhiheng Xu’s group gave direct evidence that Zika infection causes microcephaly in a mammalian animal model. They found the virus infected the neural progenitor cells, and infected brains reveal expression of genes related to viral entry, altered immune response, and cell death. Further study showed passive transfer of convalescent serum containing high-titer neutralizing antibodies to pregnant mice can not only suppress ZIKV replication but also inhibit cell death and reduction of neural progenitor cells in infected fetal brains, thus preventing microcephaly (Wang et al., Cell Res, 2016). Jianwu Dai’s group screened a functional scaffold, which showed higher endogenous neurogenesis efficiency as well as in vivo survival and neuronal differentiation rate of the grafted neural stem cells are observed (Li et al., Adv Funct Mater, 2016).
Lipid Metabolism and Development: Using state-of-theart lipidomic approach, Guanghou Shui’s group found a breakdown in DHA esterification into neural membranes may prove more detrimental than a diminished dietary supply of DHA per se (Lam et al., Oncotarget, 2016).
Vesicle Trafficking and Development: Together with Xiaojiang Hao’s group at Kunming Institute of Botany, CAS, Chonglin Yang’s group showed that protein kinase C couples activation of the TFEB transcription factor with inactivation of the ZKSCAN3 transcriptional repressor through two parallel signaling cascades. It revealed that PKC activators are viable treatment options for lysosome-related disorders (Li et al., Nat Cell Biol, 2016). Phosphatidylinositol 3-phosphate (PtdIns3P) plays a central role in endosome fusion, recycling, sorting, and early-to-late endosome conversion. Yang’s group identified two new factors, SORF-1 and SORF-2, as essential PtdIns3P regulators in Caenorhabditis elegans. These findings revealed a conserved mechanism that controls appropriate PtdIns3P levels in early-to-late endosome conversion (Liu et al., J Cell Biol, 2016).