Jun Li

Associate Professor

Biological Sciences; Biomolecular Sciences Institute

Office: OE 250B

Phone: 405-325-9385

Email: lij@fiu.edu

Curriculum Vitae


Research Areas

Mosquitoes transmit many diseases including malaria and the recent Zika virus. Li's research focuses on pathogen infection pathways using combinational approaches of genomics, chemistry and biochemistry. His group has successfully identified one novel pathway mediating Plasmodium parasite invasion in mosquitoes, a candidate protein as a malaria vaccine antigen, and a compound to block malaria transmission. As a PI, he has led several research projects supported by NSF CAREER award and NIH Research grants.

  • Using bioinformatics approaches to analyze the genome sequences and to visualize data
  • Genome-wide association approach to find mosquito genes of interest
  • Biochemical and molecular biology approaches to investigate the function of the candidate trait-related gene
  • Develop vaccines and small molecule drugs targeting the pathways

More about Dr. Li's Research

Mosquitoes transmit many diseases, including Zika and malaria. Malaria alone is responsible for about two hundred million clinical cases worldwide and kills nearly one million people each year. Malaria is caused by Plasmodium parasites that are transmitted by anopheline mosquitoes. Zika can trigger paralysis and birth defects. Inhibiting pathogen development in mosquitoes will block disease transmission. My research aims to find target genes that are essential for pathogen transmission in mosquitoes. Moreover, we develop drugs targeting these critical genes to stop disease transmission.

By genomic approaches, we discovered that the fibrinogen-related protein 1 (FREP1) is critical for malaria parasite infection in Anopheles gambiae and facilitates Plasmodium invasion in mosquitoes through interacting with gametocytes and ookinetes. Furthermore, we test the hypothesis that small molecules disrupting this interaction will prevent parasites from infecting mosquitoes. We screened a fungal extract library and obtained a candidate fungal extract of Aspergillus niger that specifically inhibited the interaction between FREP1 and P. falciparum infected erythrocytes by about 92%. Notably, feeding mosquitoes with the candidate fungal extract significantly inhibited P. falciparum infection in the mosquito midgut. A bioactive compound that prevents FREP1 from binding to gametocytes or ookinetes was isolated and identified as P-orlandin, which is neither cytotoxic nor inhibiting the development of P. falciparum gametocytes or ookinetes. Importantly, P-orlandin significantly reduced P. falciparum infection intensity in mosquitoes. In summary, we discovered FREP1 as a key gene to mediate malaria transmission. Disruption of the interaction between FREP1 and parasites effectively reduces Plasmodium infection in mosquitoes. Targeting FREP1 with small molecules is thus an effective novel approach to block malaria transmission.