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In the early Drosophila embryo, decapentaplegic (dpp), a BMP-type ligand, is key in assigning identity to all dorsal structures.
Dpp is transcribed uniformly throughout the dorsal domain, yet it forms an activity gradient in which there is a low level of signaling in the dorsal lateral regions (that will form the dorsal ectoderm tissue) and higher level of signal in the dorsal most cells (that will form the dorsal most tissue, amnioserosa).
Only about 10 cells along the dorsal midline receive high levels of signal.
How do you go from broadly expressed Dpp to highly localized signaling.
In the early embryo, the dorsal domain where Dpp is expressed in flanked by lateral region where short gastrulation, Sog, a Dpp binding protein is produced. Sog makes a complex with Dpp that inhibits Dpp signaling from spreading into the lateral domain, the neuroectoderm. At the same time, this complex, that also contains twisted gastrulation, Tsg, protects Dpp from degradation and receptor binding and internalization and allows it to diffuse.
In the dorsal domain, the complexes will encounter a protease, Tld. Tld destroys the complexes releasing the ligands. Released Dpp has 2 possible fates: it can bind to receptors and signal, or it can be captured by another Sog/Tsg complex. When the Sog levels are high, as in the lateral domain, the probability of recapture is high, whereas at the midline, Dpp is more likely to bind to its receptors and signal.
Reiterated cycles of complex formation, diffusion and destruction by Tld generate a net movement of the Dpp protein from the lateral domain towards the midline.
Sog inhibits signaling locally. But Sog complexes also help transport/ redistribute and concentrate them in region of high signaling. Without Sog there is no amnioserosa, the tissue that requires peak signaling. The balance between the positive and negative activities of Sog is regulated by the Tld protease which cleaves Sog when bound to Dpp. Without Tld excess Sog traps the ligands.
We propose that Sog’s ability to function in a transport process, as a long range BMP agonist resides, in molecular terms, in the co-substrate requirements for Tld-mediated Sog degradation.