Modeling Podocyte Biology Using Drosophila Nephrocytes

  • Paul S. HartleyEmail author
  • Richard J. Coward
Part of the Methods in Molecular Biology book series (MIMB, volume 2067)


Vertebrate podocytes are kidney glomerular cells critically required for normal renal filtration. To fulfill their role, podocytes form molecular sieves known as slit diaphragms that contribute to the glomerular filtration barrier. The disruption of podocyte biology or slit diaphragm formation in humans is a precursor to albuminuria, renal failure, and cardiovascular morbidity. Due to genetic and functional similarities, the nephrocytes of Drosophila are increasingly used to model the genetic and metabolic basis of human podocyte biology. They have the advantage that they are a much quicker system to study compared to other murine transgenic models. In this chapter we present methods to modulate and study Drosophila nephrocyte function and diaphragm formation.

Key words

Kidney Podocyte Nephropathy Drosophila Nephrocyte Slit diaphragm 


  1. 1.
    Zhuang S et al (2009) Sns and Kirre, the Drosophila orthologs of Nephrin and Neph1, direct adhesion, fusion and formation of a slit diaphragm-like structure in insect nephrocytes. Development 136(14):2335–2344CrossRefGoogle Scholar
  2. 2.
    Weavers H et al (2009) The insect nephrocyte is a podocyte-like cell with a filtration slit diaphragm. Nature 457(7227):322–326CrossRefGoogle Scholar
  3. 3.
    Hartley PS et al (2016) SPARC-dependent cardiomyopathy in Drosophila. Circ Cardiovasc Genet 9(2):119–129CrossRefGoogle Scholar
  4. 4.
    Hermle T et al (2017) Modeling monogenic human nephrotic syndrome in the Drosophila garland cell nephrocyte. J Am Soc Nephrol 28(5):1521–1533CrossRefGoogle Scholar
  5. 5.
    Ivy JR et al (2015) Klf15 is critical for the development and differentiation of Drosophila Nephrocytes. PLoS One 10(8):e0134620CrossRefGoogle Scholar
  6. 6.
    Brand AH, Perrimon N (1993) Targeted gene expression as a means of altering cell fates and generating dominant phenotypes. Development 118(2):401–415PubMedGoogle Scholar
  7. 7.
    Kimbrell DA et al (2002) The Dorothy enhancer has Tinman binding sites and drives hopscotch-induced tumor formation. Genesis 34(1-2):23–28CrossRefGoogle Scholar
  8. 8.
    Chen TW et al (2013) Ultrasensitive fluorescent proteins for imaging neuronal activity. Nature 499(7458):295–300CrossRefGoogle Scholar
  9. 9.
    Ja WW et al (2007) Prandiology of Drosophila and the CAFE assay. Proc Natl Acad Sci U S A 104(20):8253–8256CrossRefGoogle Scholar
  10. 10.
    Reiser J et al (2005) TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function. Nat Genet 37(7):739–744CrossRefGoogle Scholar
  11. 11.
    Schneider CA, Rasband WS, Eliceiri KW (2012) NIH image to ImageJ: 25 years of image analysis. Nat Methods 9(7):671–675CrossRefGoogle Scholar
  12. 12.
    Bootman MD et al (2013) Ca2+−sensitive fluorescent dyes and intracellular Ca2+ imaging. Cold Spring Harb Protoc 2013(2):83–99PubMedGoogle Scholar
  13. 13.
    Greenspan, R.J., Fly pushing: the theory and practice of Drosophila genetics. 2. 2004, New York: Cold Spring Harbor Laboratory PressGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2020

Authors and Affiliations

  1. 1.Department of Life and Environmental ScienceBournemouth UniversityPooleUK
  2. 2.Bristol Royal Hospital for Sick Children & University of BristolBristol Medical SchoolBristolUK

Personalised recommendations