Solutions For An Introduction to Genetic Analysis Chapter 12 Problem 13P

The major regulator of Galactose operon is GAL4, which express a protein called GAL4-protein. This protein specifically binds on some Upstream-activating-sequences (UAS) elements that are present prior to +1 region of the structural genes. Binding of GAL4-protein to UAS elements result expression of structural genes, therefore GAL4-protein is called the transcriptional activator protein. The pathway is as follows:

So, any mutation or structural modification in either GAL4 DNA (deoxyribonucleic acid) binding domain or activation domain results transcriptional repression of structural genes. As well as removal or changes in the UASs by addition or deletion techniques, also leads to transcriptional repression of structural genes.

The GAL3 and GAL80 regulate the Galactose operon by direct binding to GAL4-protein. The GAL3 act as an inducer or sensor in the presence or absence of galactose, whereas GAL80 inhibit the transcription by directly binding with GAL4-protein. The regulation Galactose operon by GAL3 and GAL80 is as follows:

Deletion of one GAL4-protein binding site on the GAL1 UAS element results partial expression of GAL1 in the presence galactose. This is because, even though one UAS element is deleted, there are three other UAS elements allow the binding of GAL4-protein. This will recruit the other transcriptional activator proteins and allows the transcription of GAL1 gene.

Therefore, it results partial expression of Gal1 gene.

Deletion of all four GAL4-protein binding site on the GAL1 UAS element results complete repression or inhibition of GAL1 in the presence or absence of galactose. This is because; removal of all GAL4-protein binding sites cannot allow the binding of GAL4-protein. So, intracellular galactose cannot be converted into galactose-1-Phophsate.

Therefore, it results repression or inhibition of Gal1 gene.

The Mig1 is a transcription regulatory protein, which usually recruits another repressing protein complex called Tup1. Both these proteins usually bind between the UAS elements and +1 site of GAL1 gene, and therefore inhibit the expression of GAL1 gene.

Therefore, deletion of Mig1 binding site upstream to the GAL1 gene results continues expression in the presence of galactose.

Deletion of active domain GAL4-protein results complete repression or inhibition of GAL1 gene expression in the presence or absence of galactose. This is because; removal of the active domain of GAL4-protein cannot allow the recruitment of other transcriptional factors, like TFIID, mediators and RNA polymerase too. So, the transcriptional promoting complex will not be formed.

Therefore, it results repression or inhibition of Gal1 gene.

GAL80, unusually inhibit the transcription by directly binding with GAL4-protein. So, deletion of GAL80 results absence of GAL80 protein. It cannot bind to the GAL4-protein and allows continues expression of the GAL1 gene in the presence of galactose.

Deletion of GAL41 promoter results complete repression or inhibition of GAL1 gene expression in the presence or absence of galactose. This is because; removal promoter element (TATA) cannot allow binding of the activation domain of GAL4-protein. So, recruitment of other transcriptional factors, like TFIID, mediators and RNA polymerase will not be takes place. So, the transcriptional promoting complex will not be formed.

Therefore, it results repression or inhibition of Gal1 gene.

The GAL3 is an induced molecule, in the presence of Galactose; it binds with ATP (adenosine triphosphate) and act as an allosteric modulator. This complex then binds to the GAL80-GAL4 and release GAL80, which results expression of GAL1 gene. However, deletion of GAL3 gene results absence of GAL3, and therefore GAL80-GAL4 complex remains stable and cannot allow the expression of Gal1 gene.

Therefore, it results repression or inhibition of Gal1 gene.