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Published August 1, 2007 | Accepted Version + Supplemental Material
Journal Article Open

The secreted cell signal Folded Gastrulation regulates glial morphogenesis and axon guidance in Drosophila


During gastrulation in Drosophila, ventral cells change shape, undergoing synchronous apical constriction, to create the ventral furrow (VF). This process is affected in mutant embryos lacking zygotic function of the folded gastrulation (fog) gene, which encodes a putative secreted protein. Fog is an essential autocrine signal that induces cytoskeletal changes in invaginating VF cells. Here we show that Fog is also required for nervous system development. Fog is expressed by longitudinal glia in the central nervous system (CNS), and reducing its expression in glia causes defects in process extension and axon ensheathment. Glial Fog overexpression produces a disorganized glial lattice. Fog has a distinct set of functions in CNS neurons. Our data show that reduction or overexpression of Fog in these neurons produces axon guidance phenotypes. Interestingly, these phenotypes closely resemble those seen in embryos with altered expression of the receptor tyrosine phosphatase PTP52F. We conducted epistasis experiments to define the genetic relationships between Fog and PTP52F, and the results suggest that PTP52F is a downstream component of the Fog signaling pathway in CNS neurons. We also found that Ptp52F mutants have early VF phenotypes like those seen in fog mutants.

Additional Information

© 2007 Elsevier Inc. Received for publication 14 February 2007; revised 11 May 2007; accepted 16 May 2007; Available online 24 May 2007. We are very grateful to the Wieschaus laboratory and Naoyuki Fuse for their generous gift of the Fog antibody and to Maria Leptin for sharing the fog^(4a6),hkb::fog flies prior to publication. We also thank Florenci Serras for EP52F; the Caltech Biological Imaging Centre and the Gonda Imaging Centre, UCLA for use of their confocal microscopes. Aloisia Schmid and Benno Schindelholz (former Zinn group members) discovered the Ptp52F VF phenotype. We thank them and the other present and former members of the Zinn group for helpful discussions. A.R. particularly thanks Dr. George Jackson, UCLA, in whose laboratory some part of this work was done. This work was supported by an NIH RO1 grant, NS28182, to K. Zinn and by the Gosney fellowship from Caltech to A.R.

Attached Files

Accepted Version - nihms28373.pdf

Supplemental Material - Fig1.png

Supplemental Material - Fig2.png


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