When Sp5 is in the picture, as it is in nature, it binds to Wnt3, keeping that activator from finding and binding to beta-catenin/TCF. They have a nervous system and tentacles and a working mouth. These heads, Galliot said, are totally functional. Without Sp5, the Wnt3 keeps the cycle going, and tons of heads pop up all over the regenerating hydra. 19) in the journal Nature Communications, is that when a hydra needs a new head, it releases Wnt3, which clings to beta-catenin/TCF, which activates a whole bunch of genes, including more Wnt3 and Sp5. What happens, Galliot and her colleagues reported today (Jan. "In 100 of these animals you get ectopic heads," Galliot told Live Science. To check their work, they grew hydras engineered not to express the Sp5 gene. This might sound a little strange, but it was just what the researchers were looking for: a compound that could put the brakes on an otherwise runaway feedback loop. They soon found that beta-catenin/TCF prompts the activity of Sp5 - but Sp5 also tamps down the beta-catenin/TCF signals by repressing Wnt3.
The team already knew that Wnt3 and Wnt5 got the head-growing process rolling. That left three: Wnt3, Wnt5 and a gene called Sp5. Among those five, they looked for genes that became increasingly active during regeneration.
Of those, they found only five genes that are most active at the top of the hydra's tubular body and least active at its foot, meaning they had to be specific to head growth. Of those, 124 also existed in the hydra genome. In the planarian genome, they found 440 genes that become less active when beta-catenin/TCF signals were blocked, giving them a starting point for the search for other genes involved in this cycle. They started with a close relative of hydras, planarians, or flatworms, which also regenerate. So Galliot and her colleagues went hunting.
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