How to Inform Gene Prediction for Genome - Assignment Example

EXAM 2012 Author’s name Institutional affiliation EXAM 2012 A) Features that can be used to inform gene prediction for genome Annotation is very helpful in predicting the gene in a genome since it involves the marking where the gene commences and ends while in the process identifying some of the best regions and interesting regions in the genome sequence. Additionally, Ab initio gene prediction depends on a number of signals within the sequence of the DNA such as the promoter sequences. Third, using evidence based prediction, it is universally accepted that it relies on evidence that is more than just the sequence of the DNA. In this case, the transcript sequence of the DNA is the main focal point mRNA. Finally, the information that is predicted should be in a position to be compared, lined up and combined with the sequenced genome. B Pancreatic adenocarcinoma is universally accepted as the most dangerous of the pancreatic cancer. In this case, die to its dangerous and fatal outcome, identifying people who are the most vulnerable and in the process detecting the early signs of this disease are accepted as the most crucial prevention measures. In this case, genetic risk factors and several germline are two of the most crucial ways of determining hereditary forms of pancreatic cancer. As much as susceptibility genes have not yet been identified, most researchers have acknowledged that each and every potential candidate should be tested for any potential presence of germline mutations in PALB2, BRCA2 and ATM genes. Besides, it is proven that, in some countries such as Italy, genes like CDKN2A can as well be used to describe a considerable proportion of pancreatic cancer. Question 2 Gene Knockout in yeast Gene knockout is universally accepted as a technique that is used to inactivate a gene selectively by replacing it with an allele that is mutant in nature in a then organism that is normal. Mice/ yeast knockout is very important ion unraveling cellular processes mechanisms. After exogenous DNA is absorbed by diploid yeast cells, introduced DNA and the original homologous chromosomal sites recombine in the recipient cells. Additionally, due to this targeted and specific recombination of DNA stretches that are identical that is acknowledged as homologous recombination, it is known that any gene that exists in the host’s chromosomes is able to be substituted by an allele that is mutant in nature. Moreover, the resulting combination or rather heterozygous yeast cells which is made up of one wild-type allele and one mutant allele grows normally in the end. Treatment of the recombined cells is conducted to induce sporulation and meiosis and in the process, each combined diploid cells is able to produce haploid spores that are four in number and in the end they are tested for viability. Furthermore, the first gene that went through this process based on previous research revolves around the one encoding actin which is basically a prominent cytoskeletal protein that is found in higher organisms and yeasts. However, haploid yeasts spores that basically do not possess normal actin gene are believed to generally not grow. B structure of a nucleosome A nucleosome is universally accepted as the fundamental unit of a DNA eukaryotic that is made up of a number of DNA embroiled around eight histone proteins. In this case, the copies of the historine proteins embroiled in the nucleosome include the H3. H2B, H2A and H4.Additonnaly, it acts as the principal reference point to which the DNA accessibility is determined since it is accepted as the first order of packaging DNA in the nucleus. Question 3 a) Exon definition This is basically models that entreat the linkage between the splice sites that lie across an axon which is very different from the linkage that occurs across an intron. Additionally this model is of the opinion that in the pre-mRNAs with extensive introns, it is accepted that the slicing machinery looks for a combination of closely spaced splice sites in a polarity of exons. Moreover, after the right definitions of Exons, it is then required that all those closely related exons must be juxtaposed through the interactions of the factors that acknowledge individual exons. Source: Web images: exon definitions in pre-mRNAS with large introns and small exons. b) The polyadenytation process is believed to commence as soon as the termination process of the gene transcription is complete. Additionally, the –prominent gene segment of the newly established Pre-mRNA commences by first being cleaved off by a number of proteins that combine to synthesize the Poly A tail most especially at the base of RNA’s. Besides, in some genes, it is known that this multiple proteins are responsible for adding a Polyadenytation tail at a number of several tails. In this case therefore, Poly A is assumed to offer over one transcript from one single gene which can be taken to represent an alternative polyadenytation which is otherwise called alternative splicing. Figure 2: structure of a mRNA that is mature. Figure 3: chemical structure of mRNA.source web images. C) DNA methylation is universally acknowledged as covalently adding an extra methyl group –CH3 to cytosine C in what is known as the dinucleotide or the fifth nucleotides).Additionally, for gene transcription to take place, it is argued that the gene promoter should be set up in such a way that it is readily accessible to other transcription elements coupled with other regulatory units like enhancers. In this case, methylation of the DNA works to prevent transcription factor linkage and in the process lead to structural changes in the chromatin that curb the accessibility of the transcription elements to the gene promoter. Figure 3: DNA methylation d) Histone code is accepted as a hypothesis that indicates that genetic information transcription encoded in the DNA is basically part controlled by chemical modifications that are fundamentally found in the histone proteins most especially on the unstructured end points. Additionally, Alongside DNA methylation, they together establish epigenetic code. One way that histone code functions is that they function to recruit other elements of proteins through identified proteins domains that are set aside for such purposes rather making the interlink age between underlying DNA and Histone code stable or unstable depending on the condition. Figure 5: Histone transcription initiation: source web images Question 4 The extrinsic apoptosis is a caspase pathway that is basically activated through the linkage of a receptor to a death receptor that basically works with the assistance of the adapter proteins (TRADD/FADD) to dimerization, recruitment as well as the activation of the caspase-8.In this case, the active caspase-8 is then required to interlink the apoptosis in a directly manner by cleaving and in the process activating executioner caspase b) To determine the flexibility that is needed to validate experimental results of genes that are identified and determined by expression profiling-technologies. The real-time equipment employs a Light Cycler-based real-time PCR that possess a product detection element that uses SYBE Green I Dye. It also possess a relative standard measurement element with serial dilutions of each know gene templates that permits the comparison between genes. C) MicroRNAS are highly conserv4d and small non-coding RNA molecules that are u8universally acknowledged to be involved in the expression of genes. Additionally MRNAs are also known to be transcribed by polymerases of RNA 2 and 3 generating precursors that are accepted to go through a number of cleavage events and in the process forming mature MRNA. Question 5 A MYC: is universally accepted as a primary regulator of cell proliferation, metabolism, apoptosis, differentiation and cell growth. Additionally, deregulation in the end results in breast cancer progression and development in the process, it is linked with poor outcomes. ErbB oncogene (encodes an EGF receptor oncogenic protein: is accepted biologically as a surface of the cell protein that links itself to the epidermal factor of growth. Additionally, the linkage and the binding of the surface protein produces a receptor dimerization as well as tyrosine auto-phosphorylation which in the end lead to growth and proliferation of cells which in the end lead to mutations hence resulting to lung cancer Ras oncogene: This genes are accepted as one of the well-known genes that cause some hormonal and genes imbalance hence leading to tumor development Bcl-2: development of tumor cancer needs a combination of defects that in one way or the other allows nascent neoplastic genes or cells to establish itself in a more self-sufficient manner necessary for cell proliferation and in the process; they are insensitive to cell signals that restrain cell growth. E6 oncogenic protein from papillomavirus: Specific types of genes such as the HPV, its identification and the functional variation of HPV E6 oncoproteins are believed to play a very big part in the development of cervical cancer. B Tumor cells are known to be very different from other cell types in terms of growth, cell to cell membrane, morphology, cytoskeletal structure, membrane properties, gene expression, and protein secretion. Besides, it is also clear that protein secretion and gene expression cells and molecules play a crucial part in cancer inductions. In other words, it is known that these genes encode a number of proteins that in one way or the other play a crucial part in the progression and development of cancers. Most genetic modifications that that encourage tumorigenesis revolver around dysregulatrion of G1 cell cycle progression. Additionally, one of the primary regulatory areas in GI is basically what is accepted as a growth factor dependent restriction area and another point that basically depends on the nutritional sufficiency these points help I n the reduction of proliferation of genes since they possess mTOR signals. C Tumor suppression genes can be classified as genes that encode proteins that in the process inhibit the formation of cancer tumors. Additionally, their normal role is basically to inhibit cell proliferation or play as break for the cell cycle inhibitors. Read More