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How stem cells make skin
Date:9/13/2009

e working copy of either the gene for C/EBPα or the gene for C/EBPβ was enough to ensure that skin developed properly. This means that the two proteins normally do the same job in the skin's stem cells - an unexpected redundancy, which may have arisen because there are so many stem cells in skin that a tight control on proliferation is needed to avoid problems like cancer. Or it may simply be a by-product of the fact that these two proteins have different functions in other situations, such as wound healing or repair of sunlight-induced skin damage.

One of the hallmarks of epithelial cancers - which include skin, breast, and oral cancers - is that they have genes turned on which would normally only be expressed in embryonic stem cells, and which may help cancer cells divide indefinitely. Such genes become re-expressed in the skin in the absence of C/EBPs. So, by understanding how C/EBPα and β turn off such 'stem cell' programmes, researchers hope to come a step closer to finding ways to fight such cancers.

When Nerlov and colleagues looked at how C/EBPα and -β work in the skin, they found that these proteins also regulate a number of other molecules that control skin development. Several important pathways known to control skin and hair formation were improperly activated in the mice lacking C/EBPα and -β.

"This is a very important discovery", says Nerlov. "It opens up a lot of new areas, because we can see how these proteins control virtually every other molecule known to regulate skin cell differentiation. It seems to be a key piece in the puzzle of how our skin is formed and maintained throughout life."


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Contact: Anna-Lynn Wegener
wegener@embl.de
49-622-138-7452
European Molecular Biology Laboratory
Source:Eurekalert  

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