Sloppy paired acts as the downstream target of Wingless in the Drosophila CNS and interaction between sloppy paired and gooseberry inhibits sloppy paired during neurogenesis

Citation
Km. Bhat et al., Sloppy paired acts as the downstream target of Wingless in the Drosophila CNS and interaction between sloppy paired and gooseberry inhibits sloppy paired during neurogenesis, DEVELOPMENT, 127(3), 2000, pp. 655-665
Citations number
30
Categorie Soggetti
Cell & Developmental Biology
Journal title
DEVELOPMENT
ISSN journal
09501991 → ACNP
Volume
127
Issue
3
Year of publication
2000
Pages
655 - 665
Database
ISI
SICI code
0950-1991(200002)127:3<655:SPAATD>2.0.ZU;2-0
Abstract
Wingless (Wg) and other Wnt proteins play a crucial role in a number of dev elopmental decisions in a variety of organisms. In the ventral nerve cord o f the Drosophila embryo, Wg is non-autonomously required for the formation and specification of a neuronal precursor cell, NB4-2, NB4-2 gives rise to a well-studied neuronal lineage, the RP2/sib lineage. While the various com ponents of the Wg-signaling pathway are also required for generating NB4-2, the target gene(s) of this pathway in the signal-receiving cell is not kno wn. In this paper, we show that sloppy paired 1 and sloppy paired 2 functio n as the downstream targets of the Wg signaling to generate the NB4-2 cell. Thus, while the loss-of-function mutations in wg and sip have the same NB4 -2 formation and specification defects, these defects in wg mutants can be rescued by expressing sip genes from a heterologous promoter. That sip gene s function downstream of the Wg signaling is also indicated by the result t hat expression of sip genes is lost from the neuroectoderm in wg mutants an d that ectopic expression of wg induces ectopic expression of sip. Finally, previous results show that Gooseberry (Gsb) prevents Wg from specifying NB 4-2 identity to the wg-expressing NB5-3. In this paper, we also show that g sb interacts with sip and prevents Sip from specifying NB4-2 identity. Over expression of sip overcomes this antagonistic interaction and respecifies N B5-3 as NB4-2. This respecification, however, can be suppressed by a simult aneous overexpression of gsb at high levels. This mechanism appears to be r esponsible for specifying NB5-3 identity to a row 5 neuroblast and preventi ng Wg from specifying NB4-2 identity to that cell.