The Hunger Games

The Hunger Games
awesome movie

Thursday, February 23, 2012

BOW #4


Natural selection is the primary way that organisms become better adapted to their environment. It relates to phenotype since the animals who adapt to their environment have different personality. The animals each have different genes so that relates to genotypes. Finally some reproduction may have a mutation through each offspring. A exaptation is a change in the trait during evolution.





BOW #3

If a clone originates from an existing person, who is the parent?


I believe the parent would be the person who's gene it came from. Since in a regular birth the child would have the same gene as there parents. Even if the outcome would be identical since it is a clone of the same genes, the person who's gene is in the clone should be the parent of the child. 




 Reference: http://www.google.com/imgres?q=clones&um=1&hl=en&safe=active&client=safari&sa=N&rls=en&biw=1278&bih=843&tbm=isch&tbnid=zOJv4iLso4UjaM:&imgrefurl=http://www.sodahead.com/living/lets-picture-an-scenario-if-human-cloning-was-legal-should-those-clones-be-treated-as-other-human/question-1957455/%3Fpage%3D7&docid=FPSZZdaSFOZO5M&imgurl=http://images.sodahead.com/polls/001957455/3752698267_human_cloning_answer_1_xlarge.jpeg&w=350&h=261&ei=HYNGT6e9Ms3WiALw__naDQ&zoom=1&iact=rc&dur=498&sig=106118596005183164299&page=1&tbnh=150&tbnw=201&start=0&ndsp=22&ved=1t:429,r:9,s:0&tx=140&ty=53&surl=1 

Thursday, February 16, 2012

BOW #2

Sense mutation- this is sometimes seen with a single substitution mutation when the change in the DNA base sequence results in a new codon that is still coding for the same amino acid. (All amino acids are coded for by more than one codon.)



Nonsense Mutations- the term "nonsense mutation is used because the stop codon has "no sense" for an amino acid. Nonsense mutations cause the protein to be cut off early and therefore incomplete, which usually renders it non-functional. Cystic fibrosis is a disease caused by a nonsense mutation.


Deletion Mutation- In genetics, a deletion (also called gene deletiondeficiency, or deletion mutation) (sign: Δ) is a mutation (a genetic aberration) in which a part of a chromosome or a sequence of DNA is missing. Deletion is the loss of genetic material. Any number of nucleotides can be deleted, from a single base to an entire piece of chromosome.[1] Deletions can be caused by errors in chromosomal crossover duringmeiosis. This causes several serious genetic diseases. Deletion also causes frameshift.


Insertion Mutation-In genetics, an insertion (also called an insertion mutation) is the addition of one or more nucleotide base pairs into a DNAsequence. This can often happen in microsatellite regions due to the DNA polymerase slipping. Insertions can be anywhere in size from one base pair incorrectly inserted into a DNA sequence to a section of one chromosome inserted into another.
On a chromosome level, an insertion refers to the insertion of a larger sequence into a chromosome. This can happen due to unequal crossover during meiosis.


 frameshift mutation (also called a framing error or a reading frame shift) is a genetic mutation caused by indels (insertions or deletions) of a number of nucleotides that is not evenly divisible by three from a DNA sequence. Due to the triplet nature of gene expression by codons, the insertion or deletion can change the reading frame (the grouping of the codons), resulting in a completely different translation from the original. The earlier in the sequence the deletion or insertion occurs, the more altered the protein produced is.


Point mutation-point mutation, or single base substitution, is a type of mutation that causes the replacement of a single base nucleotidewith another nucleotide of the genetic material, DNA or RNA.

Translocation Mutation-n genetics , a chromosome translocation is a chromosome abnormally caused by rearrangement of parts between non humologous chromosomes a genes fusion .may be created when the translocation join two otherwise separate genes , the occurrence of which is common in cancer .

Tuesday, February 7, 2012

My post that has nothing to do with biology #3

Oh my god....
http://www.youtube.com/watch?v=7lReemWmO5o

Extra credit blog

What topics really confused you ?
It would be the photosynthesis since there are so many steps for different cycles.

What topics do you feel very clear on?
It would be viruses since they are very easy to distinguish, since their names show which they infect. 


What lab/ activity was your favorite? Why?
It would be the burning chip since it was not hard to do in the measuring. 


What lab/activity was your least favorite? Why?
It would be the one with the petroleum ether since it was dangerous. 


If you could change something about the class to make it better, for instance the type of homework (not the amount) what would it be and why?
I would change the amount of notes since there are so much and we should focus on the main points. 

Thursday, February 2, 2012

Gene mutation WS

For gene #2- This gene encodes a protein that is one of the two components of elastic fibers. The encoded protein is rich in hydrophobic amino acids such as glycine and proline, which form mobile hydrophobic regions bounded by crosslinks between lysine residues. Deletions and mutations in this gene are associated with supravalvular aortic stenosis (SVAS) and autosomal dominant cutis laxa. Multiple transcript variants encoding different isoforms have been found for this gene.


For gene #3- Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1 or PSEN2) or the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (main component of amyloid deposits found in AD brains). Presenilins are postulated to regulate APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is thought that the presenilins are involved in the cleavage of the Notch receptor such that, they either directly regulate gamma-secretase activity, or themselves act are protease enzymes. Two alternatively spliced transcript variants encoding different isoforms of PSEN2 have been identified.


For gene #5- This gene encodes a member of the fibrillin family. The encoded protein is a large, extracellular matrix glycoprotein that serve as a structural component of 10-12 nm calcium-binding microfibrils. These microfibrils provide force bearing structural support in elastic and nonelastic connective tissue throughout the body. Mutations in this gene are associated with Marfan syndrome, isolated ectopia lentis, autosomal dominant Weill-Marchesani syndrome, MASS syndrome, and Shprintzen-Goldberg craniosynostosis syndrome. 


For gene #8- The dystrophin gene is the largest gene found in nature, measuring 2.4 Mb. The gene was identified through a positional cloning approach, targeted at the isolation of the gene responsible for Duchenne (DMD) and Becker (BMD) Muscular Dystrophies. DMD is a recessive, fatal, X-linked disorder occurring at a frequency of about 1 in 3,500 new-born males. BMD is a milder allelic form. In general, DMD patients carry mutations which cause premature translation termination (nonsense or frame shift mutations), while in BMD patients dystrophin is reduced either in molecular weight (derived from in-frame deletions) or in expression level. The dystrophin gene is highly complex, containing at least eight independent, tissue-specific promoters and two polyA-addition sites. Furthermore, dystrophin RNA is differentially spliced, producing a range of different transcripts, encoding a large set of protein isoforms. Dystrophin (as encoded by the Dp427 transcripts) is a large, rod-like cytoskeletal protein which is found at the inner surface of muscle fibers. Dystrophin is part of the dystrophin-glycoprotein complex (DGC), which bridges the inner cytoskeleton (F-actin) and the extra-cellular matrix.  

semester 2 blog #1

Protein synthesis- STEP 1: The first step in protein synthesis is the transcription of mRNA from a DNA gene in the nucleus. At some other prior time, the various other types of RNA have been synthesized using the appropriate DNA. The RNAs migrate from the nucleus into the cytoplasm.
Prior to the beginning of the protein synthesis, all of the component parts are assembled in the ribosome which is the brown/tan structure in the left graphic.

STEP 2: Initiation:
In the cytoplasm, protein synthesis is actually initiated by the AUG codon on mRNA. The AUG codon signals both the interaction of the ribosome with m-RNA and also the tRNA with the anticodons (UAC). The tRNA which initiates the protein synthesis has N-formyl-methionine attached. The formyl group is really formic acid converted to an amide using the -NH2 group on methionine (left most graphic)
The next step is for a second tRNA to approach the mRNA (codon - CCG). This is the code for proline. The anticodon of the proline tRNA which reads this is GGC. The final process is to start growing peptide chain by having amine of proline to bond to the carboxyl acid group of methinone (met) in order to elongate the peptide.
STEP 3: Elongation:
Elongation of the peptide begins as various tRNA's read the next codon. In the example on the left the next tRNA to read the mRNA is tyrosine. When the correct match with the anticodons of a tRNA has been found, the tyrosine forms a peptide bond with the growing peptide chain .
The proline is now hydrolyzed from the tRNA. The proline tRNA now moves away from the ribosome and back into the cytoplasm to reattach another proline amino acid.

Step 4: Elongation and Termination:
When the stop signal on mRNA is reached, the protein synthesis is terminated. The last amino acid is hydrolyzed from its t-RNA.
The peptide chain leaves the ribosome. The N-formyl-methionine that was used to initiate the protein synthesis is also hydrolyzed from the completed peptide at this time.
The ribosome is now ready to repeat the synthesis several more times.