Ephrin mRNA and protein expression starts at the syncytial blastoderm (about 1.5 hours after fertilization) and is ubiquitous. In situ hybridization and antibody stainings of unfertilized eggs suggest that Ephrin is not expressed maternally. At gastrulation Ephrin expression is restricted to the invaginating mesoderm and to cells lining the cephalic furrow. No mRNA or protein can be detected during germband elongation. At the start of germband retraction, expression resumes in the ventral ectoderm, ventral muscles and the CNS. In the CNS the mRNA and protein can be found in a subset of 4-6 cells at the ventral midline. In the developing brain expression can be found in medial and lateral cell clusters in the dorsal cortex and nearly all cells of the ventral cortex. After germband retraction (stage 13) the mRNA and protein are restricted to the CNS, with the highest level of expression along the outer border of the longitudinal axon tracts. The expression pattern of Ephrin complements that of Eph, a potential receptor for Ephrin. Ephrin is transcribed in neurons and the protein is confined to the cell body and very low or absent on axons. Eph is also transcribed in neurons but the protein is confined to axons (Bossing, 2002).
Both Ephrin and Eph map to the fourth chromosome, for which it is very difficult to obtain and maintain mutants by classical genetic techniques. For this reason RNAi was used to inhibit expression. RNAi has rapidly become an accepted technique for generating mutant phenotypes. In test injections of dsEphrin RNA only two out of nine injected embryos show a nearly complete loss of Ephrin, while the remainder retains about 20%-50% of wild-type expression. Therefore, it was not expected that Ephrin RNAi would lead to a mutant phenotype in all injected embryos nor that all segments per embryo would be affected. Indeed, only 65% (13/20) of embryos injected with dsEphrin showed an aberrant phenotype and in total 39% (77/200) of all segments are affected. In four injected embryos all segments were affected. The phenotypes include fused commissures, loss of commissures and breaks in the connectives. Although Ephrin RNAi impedes commissure formation, it does not interfere with the differentiation of midline glia. Injection with dsCFP or buffer does not reduce Ephrin expression but occasionally results in phenotypes similar to dsEphrin injections. However, only 30% (5/15) of dsCFP injected embryos and 23% (4/17) of buffer injected embryos show a phenotype. The number of affected segments is reduced to 6% (9/148, dsCFP) or 8% (13/167, buffer) (Bossing, 2002).
Eph RNAi also results in fused commissures, loss of commissures and breaks in the connectives. The phenotype of Eph RNAi is more severe than for Ephrin RNAi. 80% (12/15) of all embryos had a phenotype and in total 69% (98/142) of all segments were affected. In five embryos all segments were abnormal. The difference in the strength of phenotype could either indicate that additional ligands besides Ephrin signal through Eph or the difference might be caused by the efficiency of RNAi, which varies between different genes (Bossing, 2002).
RNAi against Ephrin and Eph results in the fusion or loss of commissures and breaks in the connectives. Using a general axon marker, the origin of these phenotypes is not clear. Therefore the behaviour of single axons was followed in RNAi-treated embryos. The Gal4 line CY27 primarily drives expression of UAS-taumGFP6 in 2 interneurons per hemisegment, the vMP2 and dMP2 neuron. The MP2 neurons are among the first neurons to extend their axons along the connectives. In differentiated embryos the projections of these neurons form a tight fascicle which extends close and in parallel to the midline. Loss of Ephrin or Eph causes the axons of the MP2 neurons to project aberrantly out of the CNS. In 75% of embryos (15/20, Ephrin RNAi) and 82% of embryos (14/17, Eph RNAi), MP2 axons exiting the CNS were found. In the GAL4 line CY27, additional interneurons (i.e., UMI neurons) start to express GFP in late embryogenesis. No attempt was made to examine these weak projections in detail but it was noticed that many of these interneuronal axons also project out of the CNS. Therefore, signalling between Ephrin and Eph plays a role in confining interneuronal axons to the connectives (Bossing, 2002).
In vertebrates activation of Eph receptors in axonal growth cones is able to repel axons. It was speculated that despite the structural differences between vertebrate ephrins and Ephrin, the repulsive ability of Ephrin/Eph signalling might be conserved. Ephrin expression along the outer edge of the connectives and between the commissures could create barriers preventing axon extension. Absence of these barriers would be expected to result in fusion of commissures and the exit of interneuronal axons from the CNS, as was observed in RNAi experiments. To test whether Ephrin can act as an axonal repellent, Ephrin was ectopically expressed (Bossing, 2002).
Only 4-6 out of about 20 midline neurons express Ephrin. Ectopic expression of Ephrin in all midline cells (sim-GAL4) causes fusion, severe thinning or loss of commissures without affecting midline glial cell differentiation. Single cell labelling of neural precursors reveals that ectopic Ephrin in midline cells is able to prevent the midline crossing of axons. In all clones with contralateral axons, the axons are stalled at the midline. Ectopic midline Ephrin does not affect the extension of ipsilateral axons immediately adjacent to the midline or the determination of midline neurons (judged by the expression of Engrailed, Futsch and Odd-skipped) (Bossing, 2002).
Axonal repulsion by Slit, secreted from midline cells, is one of the major mechanisms controlling axons crossing the midline. It is possible that Ephrin expression at the midline exerts its repulsive effect by upregulating the expression or secretion of Slit. To test if repulsion by Ephrin depends on Slit, Ephrin was expressed ectopically in the midline of embryos mutant for Slit and Robo1, one of the receptors for Slit. Expression of Ephrin in slit/robo double mutants forces axons out of the midline. Therefore, Ephrin/Eph signalling at the ventral midline can act independently of Slit and Robo1 (Bossing, 2002).
Ephrin is expressed in nearly all neurons but not in the longitudinal glia that enwrap the connectives. Ephrin-expressing longitudinal glia were generated by injecting UAS-Ephrin plasmids into the syncytial blastoderm of GAL4MZ1580 embryos. When longitudinal glial cells express Ephrin, breaks are observed in the connectives. The breaks are always located near the glial cell. No breaks are observed when neurons express Ephrin. GFP-expressing longitudinal glial cells also do not disrupt axon extension (UAS-tau-mGFP6 plasmid). In summary, ectopic expression of Ephrin blocks axon extension (Bossing, 2002).
Activation of Eph on axons may be the reason that axons stall at Ephrin-expressing midline cells. In that case lowering the level of Eph activation by reducing Eph expression might allow these axons to overcome this repulsion and restore the commissures. To test this hypothesis Eph expression was lowered by Eph RNAi. Embryos with ectopic midline expression of Ephrin show a strong phenotype. Only 2% (2/100) of all segments have wild-type commissures and embryos are never found in which all segments have normal commissures. Injection of dsEph RNA rescues the commissures. In 30% (8/27) of all injected embryos all segments were restored to wild type. In contrast, in all embryos injected with buffer or dsGFP, segments are found with fused or absent commissures, indicating that ectopic Ephrin is still able to repel axons. In dsEph-injected embryos 33% of all segments have wild-type commissures, whereas in control-injected embryos even fewer segments show normal commissures (Bossing, 2002).
Presumably, it is possible to rescue the commissures with Eph RNAi because dsEph-injected embryos do not always show a loss or fusion of commissures. 20% of injected embryos and 31% of all segments have no phenotype. In the rescued embryos, Eph expression might be lowered enough to overcome the repulsion by ectopic midline Ephrin but not low enough to result in fused or lost commissures (Bossing, 2002).
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date revised: 15 January 2008
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