Articles by Jingqun Ma in JoVE
Affinity-based Isolation of Tagged Nuclei from Drosophila Tissues for Gene Expression Analysis Jingqun Ma1, Vikki Marie Weake1 1Department of Biochemistry, Purdue University Drosophila tissues often contain a heterogeneous mixture of cell types. To examine gene expression in specific cell types from a particular tissue, nuclei can be genetically tagged and subsequently isolated using an affinity-based approach. Isolated nuclei can be used for downstream applications such as gene expression analysis and chromatin immunoprecipitation.
Other articles by Jingqun Ma on PubMed
Pathogenicity of Swine Influenza Viruses Possessing an Avian or Swine-origin PB2 Polymerase Gene Evaluated in Mouse and Pig Models Virology. Feb, 2011 | Pubmed ID: 21074235 PB2 627K is a determinant of influenza host range and contributes to the pathogenicity of human-, avian-, and mouse-adapted influenza viruses in the mouse model. Here we used mouse and pig models to analyze the contribution of a swine-origin and avian-origin PB2 carrying either 627K or 627E in the background of the classical swine H1N1 (A/Swine/Iowa/15/30; 1930) virus. The results showed PB2 627K is crucial for virulence in the mouse model, independent of whether PB2 is derived from an avian or swine influenza virus (SIV). In the pig model, PB2 627E decreases pathogenicity of the classical 1930 SIV when it contains the swine-origin PB2, but not when it possesses the avian-origin PB2. Our study suggests the pathogenicity of SIVs with different PB2 genes and mutation of codon 627 in mice does not correlate with the pathogenicity of the same SIVs in the natural host, the pig.
Combination of PB2 271A and SR Polymorphism at Positions 590/591 is Critical for Viral Replication and Virulence of Swine Influenza Virus in Cultured Cells and in Vivo Journal of Virology. Jan, 2012 | Pubmed ID: 22072752 Triple reassortant swine influenza viruses (SIVs) and 2009 pandemic H1N1 (pH1N1) virus contain an avian-origin PB2 with 271A, 590S, 591R, and 627E. To evaluate the role of PB2 271A, 590S, and 591R in the replication and virulence of SIV, single (1930-TX98-PB2-271T)-, double (1930-TX98-PB2-590A591A)-, and triple (1930-TX98-PB2-271T590A591A)-mutated viruses were generated in the background of the H1N1 A/swine/Iowa/15/30 (1930) virus with an avian-origin PB2 from the triple-reassortant A/swine/Texas/4199-2/98 (TX98) virus, called the parental 1930-TX98-PB2. Compared to parental virus and single- and double-mutated viruses, the triple-mutated virus replicated less efficiently in cell cultures and was attenuated in mice. These results suggest that a combination of 271A with the 590/591 SR polymorphism is critical for pH1N1 and triple-reassortant SIVs for efficient replication and adaptation in mammals.
The NA and M Genes of the 2009 Pandemic Influenza H1N1 Virus Functionally Cooperate to Facilitate Efficient Replication and Transmissibility in Pigs The Journal of General Virology. Feb, 2012 | Pubmed ID: 22337640 The 2009 pandemic H1N1 virus (pH1N1) contains NA and M genes from Eurasian avian-like swine influenza viruses (SIVs) and remaining 6 genes from North American triple reassortant SIVs. To characterize the role of pH1N1 NA and M genes in pathogenesis and transmission we evaluated their impact in the background of an H1N1 triple reassortant (tr1930) SIV in which we replaced the HA (H3) and NA (N2) of influenza A/swine/Texas/4199-2/98 virus with those from the classical H1N1 A/swine/Iowa/15/30 (1930) virus. The laboratory-adapted 1930 virus does not shed nor transmit in pigs, but the tr1930 was able to shed in infected pigs. We then substituted NA, M, or both NA and M genes of the tr1930 virus by those of pH1N1. The resulting virus with both NA and M from pH1N1 grew to significantly higher titers in cell cultures than the viruses with single NA or M from pH1N1. In a pig model, only the virus containing both NA and M from pH1N1 transmitted to and infected sentinels whereas the viruses with single NA or M from pH1N1 did not. Our results demonstrate that the right combination of NA and M genes is critical for replication and transmissibility of influenza viruses in pigs.