Gene Translicing

We will not go through the process here, but as an illustration of this “alternate splicing”, remove codons (beads) 52 - 66 from your sentence above.

Genetic transformation occurs when an organism’s genetic makeup is altered due to the introduction of new genetic information which is then incorporated into the organism’s genome. In this lab the pGLO plasmid is introduced into E. Coli bacteria, and incorporates the genes which code for the GFP and beta lactamase to the bacteria’s genome which as a result will be modified. To test the effects of the plasmid, bacteria treated with the plasmid were grown on separate plates, the first containing LB nutrient broth and ampicillin, another containing LB nutrient broth and arabinose and another containing LB nutrient broth, ampicillin and arabinose. Two more plates were grown, one with LB nutrient broth and ampicillin and the other with only the LB broth, using cells that did not contain the plasmid. Since the lab was about genetic transformation, the goal was to find which plate would glow. It was found that the plates that were not exposed to the plasmid did not glow, and the plates containing LB and arabinose and LB, ampicillin and arabinose did glow. The plates containing ampicillin, the antibiotic that kills E. coli did not grow whereas the remaining plates at least had some growth.

Genetic code is a set of rules that are stored in our DNA these codes are translated into protiens by Genetic expression. What Genetic expression does is it takes the stored information in the gentic code and and makes it into protiens and other molecules. The way the stored information is expressed determines what kind of animal it will be or whether a person will be short or tall have brown or blue eyes.So the relationship between the two would be the Genetic code is the cause and the genetic expression is the effect.

Nonsense mutation is from AAG to AAA, the amino acid will still be a lysine at that position, but it changes the recognition sequence for splicing. The intron won’t be removed.

Hereditary spastic paraplegias (HSPs) are genetically heterogeneous disorders, which are characterized by lower extremity spasticity and weakness. HSP is often caused by mutations in SPG genes, but it may be also produced by inborn errors of metabolism [1,2]. Next generation sequencing (NGS) is helpful for investigating patients in whom genetics does not fully meets the clinical presentation. We performed NGS in adult twins and found compound pathogenic mutations in MTHFR and POLG1 genes, which were consistent with metabolic changes, including hyperhomocysteinemia decreased activity of MTHFR and mitochondrial respiratory chain.

It took an additional six years for researchers to glimpse at the functions provided by SMN1. Meister et al. categorized the SMN1 protein an essential to promote correct assembly of U12 small ribonucleoproteins (snRNPs). In genetics, snRNPs are nucleic proteins responsible for the splicing of premature ribonucleic acid chains (pre-mRNA) derived from genes. Without correct splicing, mature ribonucleic acid chains (mRNAs) produce dysfunctional proteins when translated. In this case, splicing functionality of U12 - intron containing transcripts is lost, and because the transcript is wrongly coded, its translation will produce a functionless protein. Hence, loss of SMN1 results in an inability form U12 snRNPs splicing complexes, and reduced splicing functionality results in loss of U12 - intron splicing functionality (Patel and Steitz, 2003).

Recent advantages in genome-wide analyses have revealed that roughly 90% of the human genome is transcribed, yet less than 3% of the genome consists of protein-coding genes (Wu et al., 2013). The remaining genes are transcribed as noncoding RNAs (ncRNAs), which resemble mRNA in length and splicing structures yet do not encode any proteins (Wu et al., 2013). It has been debated whether all of the ncRNA transcripts are functional due to their low expression levels and low evolutionary conservation. However, many functional ncRNA have

While exome re-sequencing has proven to be advantageous in detecting putative mutations and genes associated with DCM, a gap still remains on how these genes interact and in what pathways they occupy. This has limited our understanding of what genes to target for therapeutic intervention. Little work has been done utilizing a secondary exome re-sequencing dataset for DCM to discover pathways over-represented by genes harboring putative mutations. Recently, Campbell et al., 2013, reported a TNNT2, c.517T C.T variant that segregated in the two families. [http://www.ncbi.nlm.nih.gov/sra?term=SRP022855] We propose to utilize this data in our study. The aim of the original study was to identify novel DCM putative mutations that segregated in all affected cases and not in those who were not DCM-affected. [Campbell et al., 2013] While their work helps fill an important gap in potential causes of DCM, the authors neglected to utilize exome data to determine other variants that might interact and potentially modify the effect of the c.517T C.T variant.

This study shows that 6% of the entire annotated non-coding and coding gene transcripts are overlapping with small RNAs. Highly specific subcellular positioning is found for both unannotated & annotated short RNA.

2. How do the products of alternative splicing differ and how are they similar? (1 pt)

B-statistic or log-odds that the gene is differentially expressed (only available when two groups of Samples are defined)

I agree with you that there was a conflict of interest which caused Dr. Wilson to continue with the testing even though a participant died from complications. Based on your explanations, I agree that sanctity of human life should outweigh the other principles. Plus, ethics demands that we never allow scientific examination to undermine the interests and inherent value of the distinctive human being who unselfishly enroll in such research.

The animals that belong in our ecosystem is diminishing as time goes on, many of which we have not thought of becoming endangered, are being threatened. Scientists have figured out an alternative solution to save species from being threatened by humans and natural disasters. This alternative way is gene editing, as Joseph Dussault stated in the Christian Monitor: “Gene drive, a controversial genetic editing technique through which scientists could alter or eliminate entire species, is mostly discussed alongside Zika and malaria fears” (par. 2). It can help save species as well as turn it around and attack themselves for carrying a disease. With the use of gene editing, helping preserve the species

The quantity of each product is then analyzed using qRT-PCR and the brains characterized to see if adding these genes has rescued the function of ADCK3 in the RNAi fly line

While humans are obviously different from many other mammals, such as dogs or mice, about 5% of the human genome consists of conserved sequences shared by all mammals. Interestingly, over two thirds of these sequences do not code for protein, but this does not necessarily mean that they are non-functional. One likely possibility is that these non-coding regions conserved throughout the mammalian genome function in genetic regulation. However, before determining the function of these regions within the genome, they must first be identified. After determining the conserved sequences, they can then be classified according to function. One particularly informative way to decipher the function of a non-coding DNA sequence is to determine