akaspyda33

Based on mtDNA sequences, why can't evolutionary tree separate breeds?

Some possible reasons:
1. There is not enough sequence per individual.
2. The mutation is too slow.
3. The branching tree does not reflect history (cross-breeding).

I found an interesting website that shows how we can help design new protein sequences. To design these large numbers of protein sequences, they need lots of computers. By running the Genome@home protein sequence design clients, people can lend their computers while there not using them. It simply runs alongside people's other programs and does its calculations in the unused cpus time while people are away from their desks, or even while their working on their computers. People would not notice a loss of speed, and people's computers will work as usual. All people see are small windows that show them the protein sequences their designing. If people do not want to look at them, just minimize the windows and move them to a corner of their desktops. A day or two's worth of running Genome@home is enough to design new protein sequences that the world has never seen before. All the sequences get added to the Genome@home database, so every little bit helps.

http://genomeathome.stanford.edu/

I found an interesting article that relates to what we discussed in the lecture. Scientists know that over 27% of the different-strand-overlap relationships are shared between human and mouse, compared to only ~8% conservation for same-strand-overlap relationships. More than 96% of the same-strand and different-strand overlaps that are not shared between human and mouse have both genes located on the same chromosomes in the species that does not show the overlap. But the important point is that the researchers found the causes of transition between the overlapping and non-overlapping states in the two species and found that 3' UTR change plays an important role in the transition.

http://7thspace.com/headlines/279226/overlapping_genes_in_the_human_and_mouse_genomes.html

I came across an intriguing article that talks about a horrible gene called SLC6A4. In class, we discussed if it is possible that one kind of gene can affect humans dramatically. SLC6A4 is responsible for making the protein that is targeted by all current drug treatments for depression. Studies have shown that people who inherit one form of this gene are up to four times the risk of depression if they experience unusual stresses in their lives. SLC6A4 affects risk for depression by impacting on the development of a system in the brain that mediates how negative environmental stresses and threats feel.

http://psychcentral.com/news/2008/03/13/the-role-of-heredity-in-mood-disorders/2038.html