Babak Javid

Email: bjavid{at}gmail.com (Please replace {at} to @ in the address.)

Babak Javid is a physician scientist with an interest in tuberculosis, infectious diseases and protein translational fidelity. He did his medical training in the UK, his PhD on antigen processing and presentation with Paul Lehner at Cambridge, and post-doctoral training on mycobacterial genetics with Eric Rubin at Harvard. He joined Tsinghua School of Medicine in October 2011.



Hao Li

Email: leehao{at}biomed.tsinghua.edu.cn (Please replace {at} to @ in the address.)

1) About one third of the population in the world is infected with Mtb and remain asymptomatic. Of the latent population, about 5% will develop active tuberculosis in their lifetime. We want to know that why some individuals are protected from infection while others not.
2) The mechanisms of drug resistance and tolerance in mycobacteria.
The MDX/XDR has become a big problem in the world especially in China. Also the mycobacteria become drug tolerance via natural selection. These may be big barriers to shortening TB treatment. We want to find the mechanisms behind these problems.

PhD Students


Jiayao Hong

Email: m18202736703{at}163.com (Please replace {at} to @ in the address.)

All ribosomes are not created identical. Emerging evidences reveals that ribosome heterogeneity provide another level of complexity in translation regulation in both prokaryote and eukaryote. Despite several mechanisms underlying heterogeneity, my project mainly focuses on rRNA methylation in mycobacteria. We will test the hypotheses that mycobacterial rRNA methylation level varies when encountering different states and cellular dynamics of rRNA methylation is adapted to environmental conditions by altering translation regulation.


Shizheng Zhu

Email: zhusz17{at}mails.tsinghua.edu.cn (Please replace {at} to @ in the address.)

Mistranslation has been shown to be necessary and sufficient for bacterial drug tolerance, and previous work of our lab has proved that GatCAB protein plays a role in modulating mistranslation rates in mycobacteria. I am interested in gatCAB heterogeneity in Staphylococcus aureus clinical isolates and whether these mutation we find can modulate mistranslation rate, and have further effect in mice chronic infection model.


Yayun Zheng

Email: yyzheng1995{at}126.com (Please replace {at} to @ in the address.)

tRNAs act as adapters in the genetic flow where genetic codes are transformed to functional protein. The fidelity of charging tRNAs with its cognate amino acids affects the quality of translation. We previously discovered an ambiguous tRNA gene annotated in human genome, whose anticodon decodes the codon of valine, while whose accept stem is charged with alanine. This is caused by a SNP in the anticodon of a canonical alanyl-tRNA, which is quite common in Homo sapiens populations. We tried to reveal the physiological consequence of possessing this mismatched tRNA in human body.


Zhenqi Wang

Email: wzq1994811{at}163.com (Please replace {at} to @ in the address.)

Genome-wide Association Studies(GWAS) of rifampicin-specific phenotypic resistance in Mycobacterium tuberculosis, aiming to shorten TB treatment time and to develop precision medicine for TB patients.


Biwei Wang

Email: wangbw16{at}mails.tsinghua.edu.cn (Please replace {at} to @ in the address.)

Sub-population of mycobacteria can grow and divide under rifampicin stress, which is termed as RSPR. These survivors remarkably increase treatment time so find out the mechanisms of them is very important. As a powerful screening method, Tn-seq is widely used in microorganisms also for mycobacteria. My project is investigating which genes are contributed in RSPR through different lineages by Tn-seq.


Yuemeng Chen

Email: mengmeng1054{at}163.com (Please replace {at} to @ in the address.)

Mycobacterium tuberculosis is previously proved to be able to tolerate high level mistranslation, which can contribute to the adaption to stress conditions.
For it is an obligate pathogen, it has no niche in natural environment. So I try to investigate the role of mistranslation in the interaction between mycobacteria and hosts.


Zhuo Bi

Email: bz16{at}mails.tsinghua.edu.cn (Please replace {at} to @ in the address.)

My project is to screen genes that may be involved in the misacylated tRNA mistranslation process and trying to understand the mechanism of protein translation fidelity in mycobacteria, which is an essential factor contributing to rifampicin tolerance.


Yangyang Li

Email: liyangya15{at}mails.tsinghua.edu.cn (Please replace {at} to @ in the address.)

Mycobacteria lack glutamine and asparagine aminoacyl-tRNA synthetases. Instead, they use a two-step indirect pathway, in which GatCAB, a heterotrimeric amido-transferase complex plays a crucial part. Previous studies have identified clinical isolates of Mycobacterium tuberculosis with mutated gatCAB, which had both increased mistranslation rates and tolerance to rifampicin, a first-line anti-tuberculosis drug, suggesting mycobacterial GatCAB plays a potential role in regulating adaptive mistranslation. My research interest is to characterize the enzymatic activity and stability of mycobacterial GatCAB and clinically-relevant mutants using independent in vitro biochemical and biophysical assays.


Jiazi Wang

Email: wangjz14{at}mails.tsinghua.edu.cn (Please replace {at} to @ in the address.)

Transfer RNA isodecoder genes show a large diversity in eukaryotes. But most of their functions are still unknown. I’m interested in how SNPs in human tRNAs may alter their canonical (translation) and non-canonical functions.


Yanan Chen

Email: chenyanan90618{at}163.com (Please replace {at} to @ in the address.)

Stop codons normally represent the termination signal during translation, but sometimes translation can continue through a stop codon, a mechanism known as stop codon read-through. Previous studies have shown that hundreds of Drosophila genes undergo stop codon read-through. We therefore expect to determine the precise molecular mechanism for high level stop codon read-through in Drosophila melanogaster.


Yiwei Zhang

Email: zhang-yw13{at}mails.tsinghua.edu.cn (Please replace {at} to @ in the address.)

Proteostasis is important in all domains of life, offering organisms a stable internal environment to survive and defend stress. Many cellular elements are involved in regulating proteostasis, including a protein family called small heat shock proteins (sHSPs), which widely exist across different species, yet are evolutionarily diverse. HspX is such an sHSP in M.smegmatis, and my project focus on the functional study of HspX, especially on its role in protein aggregation.


Yuxiang Chen

Email: chenyx13{at}mails.tsinghua.edu.cn (Please replace {at} to @ in the address.)

1. Mycobacterial leaderless mRNA translation regulation;
2. Ribosome heterogeneity;
3. Mechanism of increasing translation fidelity in mycobacteria.


Rongjun Cai

Email: kim32000{at}hotmail.com (Please replace {at} to @ in the address.)

In mycobacteria, tRNAAsn and tRNAGln are generated by a two-step synthesis, involving physiological misacylation to Glu-tRNAGln and Asp-tRNAAsn intermediates which are amidated to the cognate forms by GatCAB. I am focusing on the role of GatCAB in this indirect pathway to identify its potential link to relative mistranslation rate in mycobacteria. I am also interested in mechanisms to manipulate mycobacteria genetically including generation of SNPs via recombineering.

Research staff


Lei Duan

Email: duanlei87{at}126.com (Please replace {at} to @ in the address.)

As lab manager, I ensure the smooth and efficient running of the lab. I also work as Babak’s assistant and administrative aid.


Miaomiao Pan

Email: panmm99{at}163.com (Please replace {at} to @ in the address.)

I am interested in the hypothesis that a high phenotypic drug resistance in mycobacteria species is caused by high adaptive mistranslation. I am currently developing a gain of function reporter to measure the mistranslation rate using a M. smegmatis model. I will use this reporter to screen for molecules that alter mycobacterial translational fidelity.