Bio

Honors & Awards


  • Excellent Graduate, Graduate University of Chinese Academy of Sciences (2014)
  • Merit Student, Graduate University of Chinese Academy of Sciences (2013)

Professional Education


  • Doctor of Philosophy, Chinese Academy Of Sciences (2014)
  • Bachelor of Engineering, Northeast Normal University (2007)

Stanford Advisors


Research & Scholarship

Current Research and Scholarly Interests


I am interested in the biological process of RNA transcript and translation regulation, specifically by the regulation of no-coding RNA, stochastic gene expression and RNA structures.

Lab Affiliations


Publications

Journal Articles


  • The evolution of evolvability in microRNA target sites in vertebrates GENOME RESEARCH Xu, J., Zhang, R., Shen, Y., Liu, G., Lu, X., Wu, C. 2013; 23 (11): 1810-1816

    Abstract

    The lack of long-term evolutionary conservation of microRNA (miRNA) target sites appears to contradict many analyses of their functions. Several hypotheses have been offered, but an attractive one-that the conservation may be a function of taxonomic hierarchy (vertebrates, mammals, primates, etc.)-has rarely been discussed. For such an analysis, we cannot use evolutionary conservation as a criterion of target identification, and hence, have used high confidence target sites in the cross-linking immunoprecipitation (CLIP) data. Assuming that a proportion, p, of target sites in the CLIP data are conserved, we define the evolvability of miRNA targets as 1-p. Genomic data from vertebrate species show that the evolvability between human and fish is very high, at more than 90%. The evolvability decreases to 50% between birds and mammals, 20% among mammalian orders, and only 6% between human and chimpanzee. Within each taxonomic hierarchy, there is a set of targets that are conserved only at that level of evolution. Extrapolating the evolutionary trend, we find the evolvability in any single species to be close to 0%. Thus, all miRNA target sites identified by the CLIP method are evolutionarily conserved in one species, but the conservation is lost step by step in larger taxonomic groups. The changing evolvability of miRNA targets suggests that miRNA-target interactions may play a role in the evolution of organismal diversity.

    View details for DOI 10.1101/gr.148916.112

    View details for Web of Science ID 000326642500005

    View details for PubMedID 24077390

  • Rapid growth of a hepatocellular carcinoma and the driving mutations revealed by cell-population genetic analysis of whole-genome data PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Tao, Y., Ruan, J., Yeh, S., Lu, X., Wang, Y., Zhai, W., Cai, J., Ling, S., Gong, Q., Chong, Z., Qu, Z., Li, Q., Liu, J., Yang, J., Zheng, C., Zeng, C., Wang, H., Zhang, J., Wang, S., Hao, L., Dong, L., Li, W., Sun, M., Zou, W., Yu, C., Li, C., Liu, G., Jiang, L., Xu, J., Huang, H., Li, C., Mi, S., Zhang, B., Chen, B., Zhao, W., Hu, S., Zhuang, S., Shen, Y., Shi, S., Brown, C., White, K. P., Chen, D., Chen, P., Wu, C. 2011; 108 (29): 12042-12047

    Abstract

    We present the analysis of the evolution of tumors in a case of hepatocellular carcinoma. This case is particularly informative about cancer growth dynamics and the underlying driving mutations. We sampled nine different sections from three tumors and seven more sections from the adjacent nontumor tissues. Selected sections were subjected to exon as well as whole-genome sequencing. Putative somatic mutations were then individually validated across all 9 tumor and 7 nontumor sections. Among the mutations validated, 24 were amino acid changes; in addition, 22 large indels/copy number variants (>1 Mb) were detected. These somatic mutations define four evolutionary lineages among tumor cells. Separate evolution and expansion of these lineages were recent and rapid, each apparently having only one lineage-specific protein-coding mutation. Hence, by using a cell-population genetic definition, this approach identified three coding changes (CCNG1, P62, and an indel/fusion gene) as tumor driver mutations. These three mutations, affecting cell cycle control and apoptosis, are functionally distinct from mutations that accumulated earlier, many of which are involved in inflammation/immunity or cell anchoring. These distinct functions of mutations at different stages may reflect the genetic interactions underlying tumor growth.

    View details for DOI 10.1073/pnas.1108715108

    View details for Web of Science ID 000292876900066

    View details for PubMedID 21730188

  • Genome-wide misexpression of X-linked versus autosomal genes associated with hybrid male sterility GENOME RESEARCH Lu, X., Shapiro, J. A., Ting, C., Li, Y., Li, C., Xu, J., Huang, H., Cheng, Y., Greenberg, A. J., Li, S., Wu, M., Shen, Y., Wu, C. 2010; 20 (8): 1097-1102

    Abstract

    Postmating reproductive isolation is often manifested as hybrid male sterility, for which X-linked genes are overrepresented (the so-called large X effect). In contrast, X-linked genes are significantly under-represented among testis-expressing genes. This seeming contradiction may be germane to the X:autosome imbalance hypothesis on hybrid sterility, in which the X-linked effect is mediated mainly through the misexpression of autosomal genes. In this study, we compared gene expression in fertile and sterile males in the hybrids between two Drosophila species. These hybrid males differ only in a small region of the X chromosome containing the Ods-site homeobox (OdsH) (also known as Odysseus) locus of hybrid sterility. Of genes expressed in the testis, autosomal genes were, indeed, more likely to be misexpressed than X-linked genes under the sterilizing action of OdsH. Since this mechanism of X:autosome interaction is only associated with spermatogenesis, a connection between X:autosome imbalance and the high rate of hybrid male sterility seems plausible.

    View details for DOI 10.1101/gr.076620.108

    View details for Web of Science ID 000280709800008

    View details for PubMedID 20511493

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