BOW-Natural selection and exaptation

BOW What is natural selection? How does it relate to mutations, genotypes and phenotypes? What is an exaptation.


Natural selection is the gradual, nonrandom process by which biological traits become either more or less common in a population as a function of differential reproduction of their bearers. It is a key mechanism of evolution.  natural selection is dependent on the existence of mutations in the genes coding for different characteristics of an organism. Most mutations in DNA are spontaneous and random, sometimes caused by passing cosmic rays or other exposure to radiation. Mutations may also be caused by errors in the formation of the genes in the parents' gametes in sexual organisms. Additionally, "proofreading" enzymes built into many higher organisms sometimes fail, leaving an incorrect version of an organism's DNA.

Furthermore, Natural selection occurs through the mutation and recombination actions on the genome of the organism, whether through its plasmids or itself. Bare in mind that genotype, the combination of alleles of the genome, affects the phenotype, the physical appearance as a result of the genotype. Therefore, because natural selection initially occurs through the changes in the genome, natural selection acts on genotypes which may or may not have visible phenotypes.

Exaptation is a feature that performs a function but that was not produced by natural selection for its current use. Perhaps the feature was produced by natural selection for a function other than the one it currently performs and was then co-opted for its current function. For example, feathers might have originally arisen in the context of selection for insulation, and only later were they co-opted for flight. In this case, the general form of feathers is an adaptation for insulation and an exaptation for flight. (http://evolution.berkeley.edu/evosite/evo101/IIIE5cExaptations.shtml)

http://library.thinkquest.org/C004367/be2.shtml

Sem two Week Three Computer Lab - cloning

Should cloning research be regulated? How, and by whom?
     Cloning research shouldn't be regulated because without regulation scientists would be free to make advances in cloning research that would benefit society.  Since the discovery of DNA, scientific technologies have been moving forward to find ways to benefit society with its knowledge. The medical benefits of cloning have the potential to bring society to a whole new level of physical wellness.  Stem cell research promises to make way for the treatment of many disorders by replacing damaged or diseased cells with cells that are genetically compatible with the person being treated.

http://web.gccaz.edu/~mdinchak/101online_new/argument_essay_example1.htm

BOW 2 Mutations

Biology BOW
Describe the different types of mutations: sense, non-sense, deletion, insertion, framshift, point and translation.


Sense mutation: A mutation that results in a new codon still coding for the same amino acid in a polypeptide or protein. Usually due to a substitution mutation.

Non-sense mutation: A mutation that results in transcription of a nonsense codon and terminates the polypeptide or protein prematurely.

Deletion mutation: a mutation in which a part of a chromosome or a sequence of DNA is missing.   Deletions can be caused by errors in chromosomal crossover during meiosis. This causes several serious genetic diseases. Deletion also causes frame shift.

Insertion mutation:  the addition of one or more nucleotide base pairs into a DNA sequence. 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.

Frameshift mutation: 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: or single base substitution, is a type of mutation that causes the replacement of a single base nucleotide with another nucleotide of the genetic material, DNA or RNA.

Transition mutation: a point mutation that changes a purine nucleotide to another purine (A ↔ G) or a pyrimidine nucleotide to another pyrimidine (C ↔ T). Approximately two out of three single nucleotide polymorphisms (SNPs) are transitions.Transitions can be caused by oxidative deamination and tautomerization. Although there are twice as many possible transversions, transitions appear more often in genomes, possibly due to the molecular mechanisms that generate them.

Extra credit blog

     The topics that confused me the most were Fungi and Protist.  The topic that I feel very clear on was Genetics.  My favorite lab was burning cheetos and find the calories for it, because I was curious about how much calories  does each cheetos contained.  My least favorite lab was the onion lab; because I couldn't see a cell through the microscope.  One thing that I would like to change in this class was to have less reading quiz.  I prefer to take the quizlet  online instead.  Overall, I think the last semester was pretty good, and I learned lots of things from it.

2nd Semester BOW #1 (transcription, translation, protein synthesis)

BOW 1
Get a picture of transcription, translation or protein synthesis
Explain in as much detail as you can what is happening.




Transcription:    
Transcription may be broken into three major steps: 1) The DNA unwinds and unzips in the area of the gene. Enzymes match RNA nucleotides to the unzipped nitrogen bases of the gene, forming a single strand of mRNA.  2) The strand of mRNA detaches from the gene and goes out of the nucleus through one of the pores in the nuclear envelope. The DNA zips back together and winds back up.  3) The mRNA finds a ribosome where protein synthesis will happen.

Translation  :  Translation involves taking the message that's in the messenger RNA and in a sense decoding the message from the language of nucleic acids to the language of proteins or polypeptides. For translation to happen, the messenger RNA goes to the cytoplasm where it is attached to a cellular structure called a ribosome. Ribosomes are two part molecular assemblies consisting of various proteins plus a special kind of RNA called ribosomal RNA. Ribosomal RNA is involved in catalyzing some of the chemical reactions of translation.
In addition to the ribosome, another kind of RNA called tRNA carries amino acids to the mRNA when it is attached to a particular part of the ribosome's small subunit, called a binding site. A critical feature of mRNA and how it is translated is the fact that each three nucleotides in the mRNA is called a codon and it is the codon that is translated. Thus the sequence of codons corresponds to the sequence of amino acids in the polypeptide. You will see that the tRNA molecules have a set of three nucleotide bases at one end that are complementary to a corresponding codon. The bases on the tRNA are called the anti codon. This is critical because the anti codons make the connection between the codons and the correct amino acids that go with each codon.

Protein synthesis:  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.   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 -NH₂group on methionine.  

2nd Semester BOW #1 (4 Gene Sequences)

Gene 1:
Huntingtin is a disease gene linked to Huntington's
disease, a neurodegenerative disorder characterized by loss of

            striatal neurons. This is thought to be caused by an expanded,
            unstable trinucleotide repeat in the huntingtin gene, which
            translates as a polyglutamine repeat in the protein product. A
            fairly broad range in the number of trinucleotide repeats has been
            identified in normal controls, and repeat numbers in excess of 40
            have been described as pathological. The huntingtin locus is large,
            spanning 180 kb and consisting of 67 exons. The huntingtin gene is
            widely expressed and is required for normal development. It is
            expressed as 2 alternatively polyadenylated forms displaying
            different relative abundance in various fetal and adult tissues.
            The larger transcript is approximately 13.7 kb and is expressed
            predominantly in adult and fetal brain whereas the smaller
            transcript of approximately 10.3 kb is more widely expressed. The
            genetic defect leading to Huntington's disease may not necessarily
            eliminate transcription, but may confer a new property on the mRNA
            or alter the function of the protein. One candidate is the
            huntingtin-associated protein-1, highly expressed in brain, which
            has increased affinity for huntingtin protein with expanded
            polyglutamine repeats. This gene contains an upstream open reading
            frame in the 5' UTR that inhibits expression of the huntingtin gene
            product through translational repression. [provided by RefSeq, Jul
            2008].

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. [provided by RefSeq, Jul 2008].

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. [provided by
            RefSeq, Jul 2008].

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. [provided by RefSeq, Jul 2008].