for further study. This experiment allowed them to observe how the absence of GATA-3 affects skin after the birth of the mice. What they observed was a malfunctioning set of channels: the three cell layers which form the channel were nearly completely absent.
But in addition to the channel defects, the hair shaft of the grafted skin was affected: hairs grew abnormally short and thick. According to the researchers, these hair shaft irregularities were caused by both faulty hair channels as well as internal disruptions.
"We found that some of the genes in the hair shaft were misexpressed, which implies a certain level of 'cross-talk' between the shaft and channel," says Kaufman.
"This means that when the two cell types are forming, there is some communication that takes place between them, probably to ensure proper growth."
Now that the researchers have unmasked an important transcription factor controlling the fate of the hair channel, their next step is to identify the ultimate mastermind -- the extracellular signaling protein required for the activation of GATA-3. Says Fuchs, "Knowing what externally promotes hair channel lineage would round out our knowledge of the hair follicle as a whole."
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