Q and A for our research article

In our previous blog post we found an article and provided a link to the article.  After the submission of the article our teacher (Dr. Walker) has given us a series of questions that she would like us to answer based on the article and our topic.  Below is the series of questions with our answers.

1. This is a multi-part question.  To answer it, you will need to go to www.ncbi.nlm.nih.gov and follow these instructions.  From the drop-down search menu, choose "Nucleotide."  Type cebpa in the box to the right and hit "search."  Click on the Sus scrofa cebpa gene (third entry).  On the right side of the page, click "Run BLAST." On the next page, click the BLAST button at the bottom (and wait...)
a. Scroll down your results page.  Name ten other taxa (scientific and common names) that share some sequence identity with this Sus gene.
Canis (lupus) familiaris à Dog
Tursiops truncates à Bottlenose dolphin
Odobenus rosmarus à Walrus
Orcinus orca à Killer whales
Oryctolagus cuniculus à Rabbit
Pan troglodytes à Chimpanzee
Homo sapiens à Human

Papio anubis à Olive baboon

Pongo abelii à Sumatran orangutan

Callithrix jacchus à common marmoset

Otolemur garnettii à(northern) greater galago à thick-tailed bushbabies

Bos Taurus àBovine à cattle

Trichechus manatus latirostris à Florida manatee

b. What is Sus scrofa? In an evolutionary sense, why study gene regulation in this animal?
Sus scrofa is wild boar.

c. What does wild type cebpa do in these animals?  Why is it conserved across so many disparate species?
The wild type effects remission duration and overall survival.

2. According to the paper, what does the mutated cebpa allele indicate in human patients?
Patients with CEBPA mutations had higher hemoglobin levels, lower platlet counts, and higher peripheral blood (PB) blast counts.  Also they were less likely to have lymphadenopathy or extramedullary leukemia.  Other significant differences were not present regarding other clinical features between patients with mutated and unmutated CEBPA regions.

3. At what age are symptoms of adult AML typically evident in humans? Is this disease subject to natural selection? Why or why not?
The symptoms of adult AML are usually evident around 65 years of age.  Fewer than 10% of people with AML are children.  The CEBPA mutation is subject to natural selection becasue it has favorable outcomes in AML patients and can increase their lifespan and prognosis.  This is only evident in patients who plan on having children and they would pass this mutation on.  Becasue most of the symptoms of adult AML occur in older men and women, this mutation and disease are mainly evident in later age after many have already had children.  Natual selection would work on AML if the symptoms were present with adults of reproductive age and having children. Selection would act against AML and those individuals with the disease would not survive to reproduce, unless they had the CEBPA mutation.  The CEBPA mutation would be selected for because it increases the longevity and prognosis of a person with AML.

4. What does AML have to do with MDS?
AML (Acute Myeloid Leukemia) is the progression of MDS (pre-leukemia).  So most people who suffer from MDS will unfortunately progress into AML.  The comparisson is like HIV to AIDS, so most people whom have HIV will eventually transition into AIDS.