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Q: Discuss the concepts of: "PATTERN FORMATION" Also, cite examples to illustrate these concepts.
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Q: What evidence suggests that differences in monozygotic twins may be caused by epigenetic effects?
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1)
using at least one named example discuss the implication of allelic heterogeneity in single gene disorder for the presentation and progession of the disorder and its treatment
2)
discuss the importance of understanding epigenetics in improving people health
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- Discuss at least three of the disorders of focusing. What is the complete epigenetic origin which should include the genetic/biological origin and the environment influence related to these disorders of focusing.Alpha-1 antitrypsin has codominant inheritance. M genes express normal levels. S and Z genes have low expression. Which of the following is most likely to develop emphyema? A person with: 1) two M genes who does smoke 2) two S genes who does smoke 3) one M and one S gene who does not smoke 4) one M gene and one S gene who does smoke 5) two M genes who does not smoke 6) two S genes who does not smokeInborn errors of immunity (IEls) are a heterogeneous group of disorders due to genetic defects in the immune response that have a broad clinical spectrum. Diagnosis of the precise genetic cause of IEI has led to improved care and treatment of patients; however, genetic diagnosis using standard approaches is only successful in -40% of patients and is particularly challenging in "sporadic" cases without a family history. Standard genetic testing for IEl evaluates for germline changes in genes encoding proteins important for the immune response. It is now clear that IEl can also arise from de novo mutations leading to genetic variants present in germ cells and/or somatic cells. What genetic mechanism has emerged as a significant and often potentially overlooked molecular mechanism of IEI? Single nucleotide variant (SNV) - A genetic change in a single nucleotide, for example the change of a guanine (G) to an alanine (A). This may or may not be associated with altered function of the…
- Discuss briefly the effects of colchicine treatment on cells. What are the genetic implications of such effects?Some people have a genetic predisposition for developing priondiseases. Examples are described in Table 25.6. In the case ofGerstmann-Straüssler-Scheinker disease, the age of onset istypically 30–50 years, and the duration of the disease (whichleads to death) is about 5 years. Suggest a possible explanationwhy someone can live for a relatively long time withoutsymptoms and then succumb to the disease in a relativelyshort time.Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function. Hint: Loss of p53 function occurs in the majority of human tumors.
- "Changes to the p53 protein structure can be caused by differences in DNA and can affect protein function." Can you give detailed explanation why this is causation and not correlation? The explanation should be related with mutation, structure changes during protein synthesis, chemical property changes in amino acids, and functions of p53 protein.Talk about the challenges involved in determining the genetic components of polygenic illnesses. Explain complementation groups and how the biochemical underpinnings of disease are determined using them. Hereditary illnesses of genomic instability include Werner syndrome, Bloom syndrome, XP, ataxia-telangiectasia, and Fanconi anemia. Which of these ailments has molecular mechanisms behind it? Which kind of genetic instability is connected to which disorder?.Describe a potential strategy for the treatment of epigenetic disease.
- Make sure you have at minimum watched the WK11 Concepts in Context videos on Spinal Muscular Atrophy. Spinal Muscular Atrophy: “Mechanism of Splicing Regulation of Spinal Muscular Atrophy Genes” (2018) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6026014/ Abstract: “Spinal muscular atrophy (SMA) is one of the major genetic disorders associated with infant mortality. More than 90% cases of SMA result from deletions or mutations of Survival Motor Neuron 1 (SMN1) gene. SMN2, a nearly identical copy of SMN1, does not compensate for the loss of SMN1 due to predominant skipping of exon 7. However, correction of SMN2 exon 7 splicing has proven to confer therapeutic benefits in SMA patients. The only approved drug for SMA is an antisense oligonucleotide (Spinraza™/Nusinersen), which corrects SMN2 exon 7 splicing by blocking intronic splicing silencer N1 (ISS-N1) located immediately downstream of exon 7. ISS-N1 is a complex regulatory element encompassing overlapping negative motifs and…suggest reasons for why DNA mutations are not all phenotypic.A region on chromosome 6 has been linked to schizophrenia, but researchers have not found a specific gene associated with this disease. What steps would be necessary to locate the gene?
