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First published online 30 November 2006
doi: 10.1242/dev.02718

Development 134, 43-53 (2007)
Published by The Company of Biologists 2007
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Ptpmeg is required for the proper establishment and maintenance of axon projections in the central brain of Drosophila

Jessica L. Whited1, Myles B. Robichaux1, Joyce C. Yang1 and Paul A. Garrity1,2,*

1 Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
2 Biology Department, National Center for Behavioral Genomics and Volen Center for Complex Systems, Brandeis University, MS-008, 415 South Street, Waltham, MA 02454, USA.


Figure 1
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  		Fig. 1. Ptpmeg homologs, locus structure and mutations. (A) Drosophila and human Ptpmeg family proteins. The ptpmeg1 mutation is indicated. (B) ptpmeg locus with the major transcripts, ptpmeg2 insertion and ptpmeg1 mutation indicated. (C) Sequence trace showing ptpmeg1 mutation. (D) ptpmeg1 produces no detectable full-length Ptpmeg, whereas ptpmeg2 reduces Ptpmeg expression. Asterisk indicates background band. Elav is loading control.

 

Figure 2
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  		Fig. 2. ptpmeg is required for mushroom body (MB) axon patterning. (A) Diagram of the mushroom body (MB) with the neurons labeled in bold type. The locations of {alpha}, {alpha}', ß, and ß' lobes are indicated. (B,C) MB neurons visualized with OK107-Gal4;UAS-mCD8:GFP. In normal adults (B), dorsally projecting {alpha} and {alpha}' lobes are of similar thickness as medially projecting ß and ß' lobes. ß and ß' lobes project towards the midline but do not touch or cross it. In ptpmeg mutants (C), {alpha} and {alpha}' lobes are reduced, appearing thin and/or short (arrow), and ß and ß' lobes overgrow, touching the midline or fusing with the contralateral MB (bracket). (D-I) {alpha} and ß lobe axons from adult left brain hemispheres labeled with anti-Fasciclin II. E-G highlight the {alpha} lobe defects of ptpmeg mutants, including short (E, arrow), thin (F, arrow), and missing (G, asterisk) lobes. (H) {alpha} lobe reduction in ptpmeg mutants is rescued by expression of Ptpmeg in neurons using Elav-Gal4. (I) Animals with large clones of homozygous ptpmeg1 mutant MB tissue (marked in green) in otherwise heterozygous animals do not exhibit MB defects. (J) Normal spacing of ß lobe termini near midline. (K,L) ß lobes touch midline (K) or fuse with contralateral ß lobe (L) in ptpmeg mutants. (M) ß lobe defects in ptpmeg mutants are rescued by expression of wild-type Ptpmeg in neurons using Elav-Gal4. The midline is marked with arrowhead in J-M.

 

Figure 3
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  		Fig. 3. Quantification of MB axon defects in ptpmeg mutant animals. (A,B) Frequency of {alpha} and ß lobe defects in adults of the indicated genotypes. Df201 denotes Df(3L)ED201, which disrupts ptpmeg locus. ptpmeg1/TM6b and Df201/TM6c are heterozygous for ptpmeg.

 

Figure 4
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  		Fig. 4. ptpmeg is required to prevent the retraction of MB dorsal lobe axons. (A) Dorsal MB lobe defects in control and ptpmeg1/Df(3L)ED201 animals over developmental time. (B-M) Representative left hemispheres. MB neurons visualized with OK107-Gal4;UAS-mCD8:GFP. Control (B-G) and ptpmeg1/Df(3L)ED201 mutant (H-M) are shown for each age. Arrowheads in L and M indicate thin dorsal lobe in ptpmeg. Inset in L is a high magnification view of an {alpha} lobe (visualized using FasII) that has partially withdrawn. Small arrowheads denote the concentrations of material that are occasionally observed.

 

Figure 5
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  		Fig. 5. Summary of mushroom body development in wild type versus ptpmeg mutants. (A-G) Left column depicts developmental time course of mushroom bodies in wild-type animals [adapted from Lee et al. (Lee et al., 1999Go)]. Right column depicts most commonly observed defects in ptpmeg mutants. See text for details.

 

Figure 6
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  		Fig. 6. Ptpmeg protein expression in the developing and adult brain. (A) Ptpmeg expression in wild-type brain at 72 h PPF. (B) Ptpmeg expression is absent in ptpmeg1/Df(3L)ED201. (C-E) 48h PPF brain. Ptpmeg is not detectably expressed on mushroom body axons. (C) {alpha} and ß lobe axons and ellipsoid body ring axons are labeled with anti-FasII (green). Ptpmeg expression is magenta. (D-E) Ptpmeg expression (magenta), with outline of {alpha} and ß lobes and ellipsoid body superimposed in panel D. Ptpmeg is strongly expressed on ellipsoid body neurites (yellow arrowheads). (F-H) Elav-GAL4;UAS-mCD8:GFP brain at ~42 hours PPF. (F) mCD8:GFP; (G) Ptpmeg expression; (H) merge. Ptpmeg (magenta) is present on neurites, indicated by overlap with mCD8:GFP (green). Ptpmeg is also expressed in mCD8:GFP-negative regions. (I-K) Ptpmeg expression on ellipsoid body neuron cell bodies (cb) and neurites (arrowheads in K). Ptpmeg expression extends to dendritic region (ltr), but not the ellipsoid body ring. (I) Ptpmeg expression in adult. (J) Ellipsoid body neurons visualized using EB1-Gal4;UAS-mCD8:GFP. (K) Merge. (L-N) Ptpmeg expression in EB1-Gal4;UAS-mCD8:GFP;UAS-ptpmeg animal overexpressing Ptpmeg in the ellipsoid body. (L) Ptpmeg expression. (M) Ellipsoid body neurons visualized using EB1-Gal4;UAS-mCD8:GFP. (N) Merge. Note overexpressed Ptpmeg outlines cell bodies, appearing to accumulate close to the surface of the cell.

 

Figure 7
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  		Fig. 7. ptpmeg is required for normal ellipsoid body development. (A) Ellipsoid body (EB; darker part of diagram). EB axon termini form a ring labeled with anti-Fasciclin II in B-G. (B) 48h PPF control EB axon ring. (C) 48 hours PPF ptpmeg mutant EB rings are often open ventrally (arrowhead). (D) EB axons in control adult. (E,F) In ptpmeg mutant adults, EB ring is often open (arrowheads). (G) Ptpmeg expression in neurons rescues ptpmeg EB defects. (H,I) EB neurons visualized using EB1-Gal4;UAS-mCD8:GFP. (H) Control. EB cell bodies (bracket) extend a fascicle that branches to a dendritic region (asterisk) and to axons that form the ring. (I) ptpmeg mutant. EB axons are slightly defasciculated (arrow) and do not elaborate a normal ring (arrowhead). (J) ptpmeg is not required in the EB cells. Homozygous ptpmeg1 mutant EB neuron (marked in green) in otherwise heterozygous animal.

 

Figure 8
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  		Fig. 8. Ptpmeg structure-function analysis. (A,B) Rescue of ptpmeg1 phenotypes by expression of Ptpmeg transgenes using Elav-Gal4. (A) Rescue of EB defects. (B) Rescue of MB defects.

 

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© The Company of Biologists Ltd 2007