LAST BLOG

What was your favorite topic this semester? Why?
-Evolution was my most favorite topic studying about the past and how we as humans changed over time always excites me(:


What was your least favorite?
-I didn't really have a less favorite one they all interested me.

What would you change about this class if you could?
-I would have sat the kids who need more help next to ourself so they wont get distracted and help them more.More time in the lab to work on lab blogs.

What do you feel is your biggest accomplishment in biology this year ?
-I didn't really accomplish anything i did accomplish to learn that i'm not really interested in biology .

CLONING QUESTION!

 What are some of the social challenges a cloned child might face?

One of the challenges a cloned child might face is that people might mistaken him/her for the original child. Also, the clone cannot do anything that the original child could and would do in the real world, so the clone child may be hurt or jealous. And lastly, a cloned child can't have their own characteristics.

Should cloning research be regulated? How, and by whom?

Yes, I believe that cloning research should be regulated because you may not know if they use cloning for a different reason that may effect the way we live. They may be cloning people for their own use. It should be regulated by the president of the science department.

Geologic Periods

                                                                                     Triassic Period

-The Triassic is a geologic period and system that extends from about 250 to 200 Mya (million years ago). As the first period of the Mesozoic Era, the Triassic follows the Permian and is followed by the Jurassic. Both the start and end of the Triassic are marked by major extinction events. The extinction event that closed the Triassic Period has recently been more accurately dated, but as with most older geologic periods, the rock beds that define the start and end are well identified, but the exact dates of the start and end of the period are uncertain by a few million years. The Triassic period ended with a mass extinction, which was particularly severe in the oceans; the conodonts disappeared, and all the marine reptiles except ichthyosaurs and plesiosaurs. Invertebrates like brachiopods, gastropods, and molluscs were severely affected. In the oceans, 22% of marine families and possibly about half of marine genera went missing according to University of Chicago paleontologist Jack Sepkoski. This was the era of the first dinosaurs and mammals.

 

                 Cretaceous Period

-The end of the Cretaceous defines the boundary between the Mesozoic and Cenozoic eras. The Cretaceous was a period with a relatively warm climate and high eustatic sea level. The oceans and seas were populated with now extinct marine reptiles, ammonites and rudists; and the land by dinosaurs. At the same time, new groups of mammals and birds as well as flowering plants appeared. The Cretaceous ended with one of the largest mass extinctions in Earth history, the K–T extinction, when many species, including non-avian dinosaurs, pterosaurs, and large marine reptiles, disappeared.

 

 

 

 

 

 

 

                                                                                       Jurassic Period

-Jurassic constitutes the middle period of the Mesozoic era, also known as the age of reptiles. The start of the period is marked by the major Triassic–Jurassic extinction event. However, the end of the Jurassic period did not witness any major extinction event. The start and end of the period are defined by carefully selected locations; the uncertainty in dating arises from trying to date these horizons. During the Jurassic period, the primary vertebrates living in the seas were fish and marine reptiles. The latter include ichthyosaurs who were at the peak of their diversity, plesiosaurs, pliosaurs, and marine crocodiles of the families Teleosauridae and Metriorhynchidae. During this period, flowers arose and birds started roaming the Earth.

 

 

 

What is Natural Selection???

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. A mutation will tend to become more common in a population through natural selection.Phenotypes are what interact with the environment. Natural selection can distinguish between a tall plant and a short plant. So being tall (or short) may make an organism more fit.

Mutation

sense: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: A mutation which replaces a codon for an amino acid with a codon for chain termination (UAG, UAA, or UGA). 











deletion: A type of gene mutation wherein the deletion (as well as addition) of (a number of) nucleotide(s) causes a shift in the reading frame of the codons in the mRNA, thus, may eventually lead to the alteration in the amino acid sequence at protein translation.

insertion: Mutations that result in the addition of extra DNA are called insertions. 

frameshift: In a frame shift mutation, one or more bases are inserted or deleted, the equivalent of adding or removing letters in a sentence.





















point:  A point mutation is a simple change in one base of the gene sequence. This is equivalent to changing one letter in a sentence, such as this example, where we change the 'c' in cat to an 'h':

translocation: Translocations are the transfer of a piece of one chromosome to a nonhomologous chromosome. Translocations are often reciprocal; that is, the two nonhomologues swap segments.

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.

Name That Gene!!!

 Gene Sequence 1: ATG GCG ACC CTG GAA AAA GCT GAT GAA GGC CTT CGA GTC CCT CAA GTC CTT CCA GCA GCA GCA GCA GCA GCA GCA GCA GCA GCA GCA GCA GCA GCA GCA GCA GC

Summary:

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 Sequence 2: GCG GGT CTG ACG GCG GCG GCC CCG CGG CCC GGA GTC CTC CTG CTC CTG CTG TCC ATC CTC CACCCC TCT CGG CCT GGA GGG GTC CCT GGG GCC ATT CCT GGT GGA GTT CCT GGA GGA GTC TT

Summary:

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 Sequence 3:  ATG CTC ACA TTC ATG GCC TCT GAC AGC GAG GAA GAA GTG TGT GAT GAG CGG ACG TCC CTA ATG TCG GCC GAG AGC CCC AGC CCG CGC TCC TGC CAG GAG GGC AGG CAG GGC CCA GAG GAT GGA G

Summary:

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 Sequence 5: GGG GCG GAC GCC AAT TTG GAG GCT GGG AAC GTG AAG GAA ACC AGA GCC AGT CGG GCC

ATG CGT CGA GGG CGT CTG CTG GAG ATC GCC CTG GGA TTT ACC GTG CTT TTA GCG TCC TAC ACG AGC 

Summary: 

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]