The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Activation of the mec-3 promoter in two classes of stereotyped lineages in Caenorhabditis elegans.

The mec-3 gene of Caenorhabditis elegans encodes a homeodomain protein and is expressed in one of two cells upon asymmetric cell division. As a result of asymmetric mec-3 expression, the two sister cells express different fates, so mec-3 is a likely target for the machinery that mediates asymmetric cell division. The unc-86 gene encodes a homeodomain protein of the POU family, which activates mec-3 by binding to its promoter. The ten mec-3-expressing cells are a subset of the anterior daughters of UNC-86-containing cells. Posterior daughters of UNC-86-containing cells do not express mec-3, even though the UNC-86 protein is distributed into both daughter cells. Lineages that express the unc-86 and mec-3 genes can be grouped into two types: in Type I lineages, UNC-86 protein is first made in the immediate parent of the terminal mec-3-expressing cell, while in Type II lineages, UNC-86 is first made in the grandparent of the terminal mec-3-expressing cell. The purpose of experiments presented here is to understand the relationship between the mec-3 expression patterns in each type of lineage, and to determine the fundamental activity pattern of the mec-3 promoter. We find that in the Type I V5.pa lineage, mec-3-lacZ is first synthesized in the terminal PVDR neuron, one cell division after unc-86 is expressed. mec-3 expression in PVDR can occur by transcriptional regulation alone; segregation of the mec-3 RNA or protein is not required to explain the asymmetric expression of mec-3. In the Type II Q lineage, the mec-3 promoter activity can be detected in the immediate anterior daughter of the first unc-86-expressing cell, but when this cell divides, mec-3 is expressed in only one of its daughters at later times. It seems likely that, in the short-lived immediate anterior daughter cell in Type II lineages, mec-3 product does not accumulate to levels that can influence subsequent events. Our results suggest that the mec-3 promoter is activated in all anterior daughters of unc-86-expressing cells.[1]

References

 
WikiGenes - Universities