Professional Education

  • Doctor of Philosophy, Tsinghua University (2020)
  • Bachelor of Science, Sichuan University (2013)
  • PhD, Tsinghua University, Microbiology, Molecular Biology (2020)
  • BS, Sichuan University, Biology (2013)

Stanford Advisors

Contact

  • Academic
    chenyx8@stanford.edu
    University - Scholar Department: Genetics Position: Postdoctoral Scholar

Additional Info

Lab Affiliations

All Publications

  • RAPIDASH: Tag-free enrichment of ribosome-associated proteins reveals composition dynamics in embryonic tissue, cancer cells, and macrophages. Molecular cell Susanto, T. T., Hung, V., Levine, A. G., Chen, Y., Kerr, C. H., Yoo, Y., Oses-Prieto, J. A., Fromm, L., Zhang, Z., Lantz, T. C., Fujii, K., Wernig, M., Burlingame, A. L., Ruggero, D., Barna, M. 2024

    Abstract

    Ribosomes are emerging as direct regulators of gene expression, with ribosome-associated proteins (RAPs) allowing ribosomes to modulate translation. Nevertheless, a lack of technologies to enrich RAPs across sample types has prevented systematic analysis of RAP identities, dynamics, and functions. We have developed a label-free methodology called RAPIDASH to enrich ribosomes and RAPs from any sample. We applied RAPIDASH to mouse embryonic tissues and identified hundreds of potential RAPs, including Dhx30 and Llph, two forebrain RAPs important for neurodevelopment. We identified a critical role of LLPH in neural development linked to the translation of genes with long coding sequences. In addition, we showed that RAPIDASH can identify ribosome changes in cancer cells. Finally, we characterized ribosome composition remodeling during immune cell activation and observed extensive changes post-stimulation. RAPIDASH has therefore enabled the discovery of RAPs in multiple cell types, tissues, and stimuli and is adaptable to characterize ribosome remodeling in several contexts.

    View details for DOI 10.1016/j.molcel.2024.08.023

    View details for PubMedID 39260367

  • Mechanical morphotype switching as an adaptive response in mycobacteria. Science advances Eskandarian, H. A., Chen, Y., Toniolo, C., Belardinelli, J. M., Palcekova, Z., Hom, L., Ashby, P. D., Fantner, G. E., Jackson, M., McKinney, J. D., Javid, B. 2024; 10 (1): eadh7957

    Abstract

    Invading microbes face a myriad of cidal mechanisms of phagocytes that inflict physical damage to microbial structures. How intracellular bacterial pathogens adapt to these stresses is not fully understood. Here, we report the discovery of a virulence mechanism by which changes to the mechanical stiffness of the mycobacterial cell surface confer refraction to killing during infection. Long-term time-lapse atomic force microscopy was used to reveal a process of "mechanical morphotype switching" in mycobacteria exposed to host intracellular stress. A "soft" mechanical morphotype switch enhances tolerance to intracellular macrophage stress, including cathelicidin. Both pharmacologic treatment, with bedaquiline, and a genetic mutant lacking uvrA modified the basal mechanical state of mycobacteria into a soft mechanical morphotype, enhancing survival in macrophages. Our study proposes microbial cell mechanical adaptation as a critical axis for surviving host-mediated stressors.

    View details for DOI 10.1126/sciadv.adh7957

    View details for PubMedID 38170768

https://orcid.org/0000-0002-3231-2047