Haploinsufficient locus (not associated with strong haplolethality or haplosterility).

S protein appears to traffic the spi precursor while cycling between the endoplasmic reticulum and late endosomes in S[[2]]R[+] cells.

Cleavage of the S protein (by rho or ru protein) leads to its inactivation as a spi chaperone.

S may have a role in spi processing or transmission.

S interacts directly with spi.

S is required to export spi protein from the endoplasmic reticulum to the Golgi apparatus.

rho and S function in a synergistic and co-dependent manner, that is independent of spi, to promote vein development through the Egfr/MAPK signalling pathway.

Four EMS induced alleles were identified in a screen for mutations affecting commissure formation in the CNS of the embryo.

S protein is likely to be involved in spi ligand processing.

6 "ES2-4" alleles of S have been isolated in a screen for dominant modifiers of the sina^GMR.PN eye phenotype.

Genetic interaction studies suggest the S gene may participate in Egfr signalling in the ovary.

In vivo culture of mutant discs from genotypes that are normally embryonic lethal demonstrates S has no role in wing disc growth.

Identified in a genetic screen for modifiers of the phl::tor^12D.sev rough eye mutant phenotype.

The function of spi, rho and S appears to be non-autonomous; expression of the precursor only in the midline is sufficient for patterning the ventral ectoderm. Facilitating the expression of spi, rho and S is the only sim-dependent contribution of the midline to patterning the ventral ectoderm, since the mutant sim ectodermal defects can be overcome by expression of secreted spi in the ectoderm. These results suggest a mechanism for generating a graded distribution of secreted spi, which may subsequently give rise to graded activation of Egfr in the ectoderm.

Studies of interaction between argos and members of the Ras/MAPK pathway demonstrate the argos gene product is a negative regulator of signal transduction that acts upstream of the Ras/MAPK cascade.

S mutants show a suppressive effect on mutant argos phenotypes.

The spi product triggers the Egfr signaling cascade. Graded activation of the Egfr pathway may normally give rise to a repertoire of discrete cell fates in the ventral ectoderm and graded distribution of spi may be responsible for the graded activation. The rho and S products may act as modulators of Egfr signaling. Epistatic relationships suggest that rho and S may normally facilitate processing of the spi precursor.

Alleles of S and of ro have been identified in a screen for abnormal numbers of R8 cells.

The interaction of rap and rg with S is synergistic and dosage sensitive.

Mutations can act as dominant modifiers of the activated N eye phenotype (FBrf0064452).

Rescue analysis of mutant alleles with heat inducible S constructs shows that the asteroid mutants are a viable class of alleles in the S gene.

Loss of function mutations in S act as suppressors of R7 development in a sensitized genetic background involving Sos, and overexpression of S enhances R7 development in this genetic background.

S plays an early role in photoreceptor development, and interacts with Egfr in the developing eye. S may also have a later role in photoreceptor development including the recruitment of the R7 cell through the sev pathway.

The differentiation of individual mesectoderm cells (MECs) lineages is traced. S is necessary for determining the correct number of cells in many neuronal MEC lineages. The correct number of midline glia are determined but later become apoptotic in embryos mutant for S.

S function is required for the reception of a signal and/or the execution of a developmental program that leads to the neuronal differentiation of photoreceptors R8, R2 and R5. S is also required for the formation of the wing veins. Dosage-dependent genetic interaction between S and sev, Ras85D and Sos (involved in receptor tyrosine kinase signalling) supports a role for S in cell-cell signalling.

Molecular data and phenotypic interactions are consistent with the interpretation that S and ast mutations are lesions within the same gene or within genes that are functionally related.

rho gene product acts synergistically with Egfr signalling components.

A screen that identified Dominant suppressors of the wing phenotype associated with Dl^9P and Dl^FE32 identified 14 new S alleles.

S mutants have a weak salivary placode phenotype: the placodes are separated by two cells instead of four.

Zygotically active locus involved in the terminal developmental program in the embryo.

rho, pnt, S and spi all function in the formation of the same chordotonal organs.

ve, vn, ci, cg, svs, ast (S), H, Vno and vvl belong to the vein phenotypic group (Puro, 1982, D. I. S. 58:205--208 ) within the 'lack-of-vein' mutant class. Loss-of-function alleles at these loci remove stretches of veins in two or more longitudinal veins. Double mutations within members of this group remove all veins, have smaller, slightly lanceolate wings, no sensilla and extra chaetae.

Eyes slightly smaller and narrower than wild type; texture somewhat rough from rounded, irregular facets. Arrangement of hairs on surface of eye irregular. S/ast has small rough eyes; S ast/+ + is like S/+. Enhanced by E(S); partially suppresses px and net (Bedichek, 1936; Lewis, 1945). Homozygote dies in late embryonic stage (Sivertzev-Dobzhansky, 1927; Sonnenblick and Huettner, 1938). A member of the so-called spitz group of mutants; embryos lack structures derived from ventral-lateral region of blastoderm. Denticle bands narrow and ventral arms of head skeleton fused. Anal pads reduced. Transverse commissures of ventral nervous system reduced; Keilin organs, maxillary and antennal sense organs strongly reduced. Lethal in homozygous clones in female germ line (Nusslein-Volhard, Wieschaus and Kluding, 1984; Mayer and Nusslein-Volhard, 1988).

Source for merge of: S l(2)k09538

Source for merge of: S l(2)c00080