Hi. could anyone help me with some revision/learning? I missed these lectures due to illness -- knowing these things would give me a good starting point for the solid revision:

 

1/where do tandem repeats come from? I know that they cause recombination misalinments, which can reslut in their elongation, but this only elongaes existing TNRs: what actually causes them in the first place?

 

2/is there any difference between the structural effects of trinucleotide repeats and tetranucleotide repeats? eg, mononucleotide repeats can cause bends in the dna helix, triNRs can cause complex dna structures (like hair pins etc)... am i right in assuming that any oligonucleotide repeats have similar properties to triNRs?

 

3/ other than telomeres, are there any other functional TRs?

 

Cheers

1. Random 'evolution' or left over pieces of transposon/provirus. Only a few copies is enough to cause misalignment and repetition.

 

2. Short oligo repeats can cause complex structures (if they're too long, the delta G for unwinding the DNA is too high). Single nucleotide repeats just bend the DNA since there's no complimentary sequence except what they're already bound to.

 

3. Ribosomal genes (but those are little bit long). The short TNRs must assist in crossing over, though, since it's very easy to 'align' (read: misalign) them. That's why they tend to increase or decrease in size.

Cheers zyncod -- i was really having trouble finding those things out