High impact information on sog

• Signaling by these ligands is regulated at the extracellular level by the BMP binding proteins Sog and Tsg [1].
• Facilitated transport of a Dpp/Scw heterodimer by Sog/Tsg leads to robust patterning of the Drosophila blastoderm embryo [1].
• Dorsal-ventral patterning within the ectoderm of the Drosophila embryo requires seven zygotic genes, including short gastrulation (sog) [2].
• In this report we provide the first direct evidence that sog plays a local role in the lateral region of the blastoderm embryo to oppose Dpp activity in the neuroectoderm [3].
• We propose that one or more of these cysteine repeats can be liberated by proteolytic cleavage of the primary Sog protein [4].

Biological context of sog

• In accord with this result, coexpression of intact Sog and Tsg in developing wings generates a phenotype very similar to that of Supersog [5].
• Here, we provide evidence that maternal Sog and Dpp proteins are secreted into the perivitelline space where they remain until early embryogenesis to modulate Cactus degradation, enabling their dual function in patterning the eggshell and embryo [6].
• Here we show that the misexpression of sog using the even-skipped stripe-2 enhancer redistributes Dpp signalling in a mutant background in which dpp is expressed throughout the embryo [7].
• Local inhibition and long-range enhancement of Dpp signal transduction by Sog [7].
• These results suggest that the Sog inhibitor and Brk repressor work in concert to establish sharp dorsolateral limits of gene expression [8].

Anatomical context of sog

• These data strongly support the view that the primary phylogenetically conserved function of the Drosophila sog and dpp genes and the homologous Xenopus chordin and BMP-4 genes is to subdivide the primitive embryonic ectoderm into neural versus non-neural domains [3].
• RNA interference-mediated depletion of the spider sog gene led to a nearly complete loss of ventral structures, including the axial ventral midline and the central nervous system [9].
• However, Drosophila Sog makes only minor contributions to the development of ventral structures that hypothetically correspond to the vertebrate dorsum where the axial notochord forms [9].
• Normal sog expression is required in the zygote, but not in the mother for normal embryonic development and viability [10].

Associations of sog with chemical compounds

• Clonal analysis reveals that integrin mutations affect the trajectory of veins inside the provein domain and/or their width and that misexpression of sog can alter the behavior of cells in such clones [11].

Regulatory relationships of sog

• In contrast, sog is expressed in complementary intervein cells and suppresses vein formation. sog and dpp function during the same phenocritical periods (i.e. 16-28 hours after pupariation) to influence the vein versus intervein cell fate choice [12].

Other interactions of sog

• These data support the view that Sog is a dedicated Dpp antagonist [12].
• Consistent with this finding, sog(- )and tsg(-) mutants exhibit similar dorsal patterning defects during early gastrulation [5].
• We demonstrate that sog and cv can have both positive and negative effects on BMP signaling in the wing [13].
• We propose that the specific catalytic properties of Tlr and Tld have evolved to achieve the proper balance between the inhibitory and positive activities of Sog in the PCV and early embryo, respectively [14].
• Finally, we show that Sog diffusion into provein regions and the reticular pattern of extracellular Sog distribution in wild-type wings requires mys and mew function [11].

References