Plasmodium falciparum genetic crosses in a humanized mouse model (original) (raw)

References

  1. Hayton, K. et al. Cell Host Microbe 4, 40–51 (2008).
    Article CAS Google Scholar
  2. Ranford-Cartwright, L.C., Hayton, K.L. & Ferdig, M.T. in Malaria Parasites: Comparative Genomics, Evolution and Molecular Biology (eds. Carlton, J.M., Perkins, S.L. & Deitsch, K.W.) Ch. 6, 127–144 (Caister Academic Press, 2013).
  3. Walliker, D. et al. Science 236, 1661–1666 (1987).
    Article CAS Google Scholar
  4. Rodhain, J. & Jadin, J. Ann. Soc. Belges Med. Trop. Parasitol. Mycol. 44, 531–535 (1964).
    CAS PubMed Google Scholar
  5. Vaughan, A.M. et al. J. Clin. Invest. 122, 3618–3628 (2012).
    Article CAS Google Scholar
  6. Sá, J.M. et al. Proc. Natl. Acad. Sci. USA 106, 18883–18889 (2009).
    Article Google Scholar
  7. Sullivan, J.S. et al. Am. J. Trop. Med. Hyg. 69, 593–600 (2003).
    Article Google Scholar
  8. Vaughan, A.M. et al. Mol. Biochem. Parasitol. 186, 143–147 (2012).
    Article CAS Google Scholar
  9. Trager, W. & Jensen, J.B. Science 193, 673–675 (1976).
    Article CAS Google Scholar
  10. Kaushal, D.C., Carter, R., Miller, L.H. & Krishna, G. Nature 286, 490–492 (1980).
    Article CAS Google Scholar
  11. Su, X. et al. Science 286, 1351–1353 (1999).
    Article CAS Google Scholar
  12. Colwell, R.K. et al. J. Plant Ecol. 5, 3–21 (2012).
    Article Google Scholar
  13. Dondorp, A.M. et al. N. Engl. J. Med. 361, 455–467 (2009).
    Article CAS Google Scholar
  14. Cheeseman, I.H. et al. Science 336, 79–82 (2012).
    Article CAS Google Scholar
  15. Jiang, H. et al. Genome Biol. 12, R33 (2011).
    Article CAS Google Scholar
  16. Ariey, F. et al. Nature 505, 50–55 (2014).
    Article Google Scholar
  17. Takala-Harrison, S. et al. Proc. Natl. Acad. Sci. USA 110, 240–245 (2013).
    Article CAS Google Scholar
  18. Azuma, H. et al. Nat. Biotechnol. 25, 903–910 (2007).
    Article CAS Google Scholar
  19. Vaughan, A.M. et al. Cell. Microbiol. 11, 506–520 (2009).
    Article CAS Google Scholar
  20. Mita, T. & Jombart, T. Parasitol. Int. 64, 238–243 (2015).
    Article Google Scholar
  21. Reilly Ayala, H.B., Wacker, M.A., Siwo, G. & Ferdig, M.T. BMC Genomics 11, 577 (2010).
    Article Google Scholar
  22. Oyola, S.O. et al. BMC Genomics 13, 1 (2012).
    Article CAS Google Scholar
  23. Quail, M.A. et al. Nat. Methods 9, 10–11 (2012).
    Article CAS Google Scholar
  24. Li, H. & Durbin, R. Bioinformatics 25, 1754–1760 (2009).
    Article CAS Google Scholar
  25. DePristo, M.A. et al. Nat. Genet. 43, 491–498 (2011).
    Article CAS Google Scholar
  26. Broman, K.W., Wu, H., Sen, S. & Churchill, G.A. Bioinformatics 19, 889–890 (2003).
    Article CAS Google Scholar

Download references

Acknowledgements

We thank the Center for Infectious Disease Research (formerly Seattle BioMed) insectary and vivarium for mosquito and rodent care, respectively, as well as R. Garcia and M. McDew-White at the Texas Biomedical Research Institute for technical assistance. We thank S. Mikolajczak, E. Wilson and J. Bial for ongoing FRG huHep mouse discussions and M. Macarulay and K. Ushimaru for help with parasite cloning. Thanks also to A. Kaushansky for help with graphics. NIH grants R21 AI 115194–01 to A.M.V. and M.T.F., R37 AI 048071 to T.J.C.A. and Chemistry-Biochemistry-Biology Interface Training Fellowship T32 GM075762 to R.S.P. supported this work, as did Seattle BioMed internal funds to S.H.I.K. The AT&T Genomics Computing Center at Texas Biomedical Research Institute is supported by the AT&T Foundation and the US National Center for Research Resources (NCRR) grant number S10 RR029392, and laboratory work was conducted in facilities constructed with support from Research Facilities Improvement Program grant C06 RR013556 and RR017515 from NCRR.

Author information

Authors and Affiliations

  1. Center for Infectious Disease Research (formerly Seattle Biomedical Research Institute), Seattle, Washington, USA
    Ashley M Vaughan, Nelly Camargo, Matthew Fishbaugher & Stefan H I Kappe
  2. Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana, USA
    Richard S Pinapati, Lisa A Checkley, Carolyn A Hutyra & Michael T Ferdig
  3. Texas Biomedical Research Institute, San Antonio, Texas, USA
    Ian H Cheeseman, Shalini Nair & Timothy J C Anderson
  4. Shoklo Malaria Research Unit, Mahidol-Oxford Tropical Medicine Research Unit, Mahidol University, Mae Sot, Thailand
    François H Nosten
  5. Department of Global Health, University of Washington, Seattle, Washington, USA
    Stefan H I Kappe

Authors

  1. Ashley M Vaughan
  2. Richard S Pinapati
  3. Ian H Cheeseman
  4. Nelly Camargo
  5. Matthew Fishbaugher
  6. Lisa A Checkley
  7. Shalini Nair
  8. Carolyn A Hutyra
  9. François H Nosten
  10. Timothy J C Anderson
  11. Michael T Ferdig
  12. Stefan H I Kappe

Contributions

A.M.V., S.H.I.K. and M.T.F. conceived, initiated and supervised the project. A.M.V., S.H.I.K., T.J.C.A., R.S.P. and M.T.F. designed experiments and wrote the manuscript. A.M.V., N.C., M.F., L.A.C., R.S.P., I.H.C., S.N. and C.A.H. carried out the experiments. F.H.N. and T.J.C.A. supplied parasites. A.M.V., S.H.I.K., I.H.C., T.J.C.A., R.S.P. and M.T.F. analyzed results.

Corresponding authors

Correspondence toMichael T Ferdig or Stefan H I Kappe.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Integrated supplementary information

Supplementary Figure 1 Proof of recombination from the NF54HT-GFP–luc × GB4 cross.

Progeny from the NF54HT-GFP–luc (N) × GB4 (G) cross were cloned after selection with WR99210 (NF54HT-GFP–luc is resistant) and chloroquine (GB4 is resistant). Primers specific for the GFP–luc integration and the chloroquine resistance-associated (CQR) allele pfcrt were used to amplify genomic DNA from ten progeny (1 through 10). Agarose gel electrophoresis shows the presence of both the GFP-luc integration (a) and following ApoI digestion, the presence of the CQR allele, in all progeny (b). Full gels are presented to the right of each panel.

Supplementary Figure 2 Segregation of 7,536 SNPs and microsatellites (MSs) in 14 progeny from the P. falciparum NF54HT-GFP–luc × NHP* experimental genetic cross.

As an example, chromosome 11 is shown in the main body of the text (Fig. 2). Each row represents an individually sequenced chromosome from one of the 14 progeny. Haplotypes inherited from NHP* are shown in black and those from NF54HT-GFP–luc in red, while microsatellite markers from NHP* are shown in yellow and those from NF54HT-GFP–luc in blue. Seventeen of the 22 MS developed for the study are shown; the remaining five were invariant in the two parents. Chromosome regions in white mark the position of recombination breakpoints. Chromosomes are shown from the first to the last genotyped marker, and therefore do not start at zero base pairs. The grey tick marks along the top of each chromosome indicate the position of the segregating SNPs, while the scale (in base pairs) is shown at the base of the figure.

Supplementary Figure 3 Pairwise allele sharing among 14 progeny from the P. falciparum NF54HT-GFP–luc × NHP* experimental genetic cross.

With Mendelian segregation, progeny are expected to share on average 50% of markers that are identical by descent. We calculated the proportion of segregating SNPs at which each of 91 pair-wise combinations of progeny genotypes differ, and plotted the frequency distribution of these values. Segregation was normally distributed and centered on 52% (mean = 52%, s.d. = 8.03, Shapiro-Wilk test, P = 0.27, W = 0.98).

Supplementary information

Source data

Rights and permissions

About this article

Cite this article

Vaughan, A., Pinapati, R., Cheeseman, I. et al. Plasmodium falciparum genetic crosses in a humanized mouse model.Nat Methods 12, 631–633 (2015). https://doi.org/10.1038/nmeth.3432

Download citation