Briefly explain the differences between somatic and germ line mutations. Also, tell us what kind of differences you expect to see between autosomal and X-linked mutations which lead to genetic disorders
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A:
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Q: What are the differences between autosomal and X-linked mutations which lead to genetic disorders
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Briefly explain the differences between somatic and germ line mutations. Also, tell us what kind of differences you expect to see between autosomal and X-linked mutations which lead to genetic disorders
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- Lauren reports that she had a maternal male cousin (through a maternal aunt) and a maternal great uncle (maternal grandmother’s brother) both pass away from the same x-linked lethal condition. Both affected individuals did not have genetic testing. Lauren has a normal carrier screen for x-linked lethal conditions, which you know identifies 40% of causative mutations. If Lauren is currently pregnant with a male child, what is the chance that this child will have the condition?Duchenne Muscular Dystrophy (DMD) is a disease that manifests in muscle weakness. It exhibits X-linked recessive inheritance pattern. The dystrophin gene is large and can have many different mutations along the DNA. From the following mutations between the gene sequence (DNA template strand) of a healthy male and an affected brother determine if they would affect the production of mRNA or the sequence of the protein. Base your analysis on the position of the mutation in the transcription unit, and the impact of the change on the codons. Mutation 1: Position -6 Healthy individual A Affected brother C Group of answer choices A. Normal mRNA, normal protein B. No mRNA produced (promoter affected) C. Abnormal mRNA, affected protein D. Normal mRNA, affected protein Base your analysis on the position of the mutation in the transcription unit, and the impact of the change on the codons.Theodor Boveri predicted that malignancies would often be associated with chromosomal mutation. What lines of evidence substantiate this prediction?
- The gene causing Coffin-Lowry syndrome (OMIM 303600) was recently identified and mapped on the human X chromosome. Coffin-Lowry syndrome is a rare disorder affecting brain morphology and development. It also produces skeletal and growth abnormalities, as well as abnormalities of motor control. Coffin-Lowry syndrome affects males who inherit a mutation of the X-linked gene. Most carrier females show no symptoms of the disease but a few carriers do. These carrier females are always less severely affected than males. Offer an explanation for this finding.How do germ-line mutations differ from somatic mutations? Germ-line mutations are reversible, while somatic mutations are not. Germ-line mutations result in mutant gametes, while somatic mutations do not. Germ-line mutations occur during DNA replication, while somatic mutations do not. Germ-line mutations result in cancers, while somatic mutations do not. Germ-line mutations involve small changes to DNA such as base-pair substitutions, while somatic mutations involve large deletions.Fragile X syndrome why is interesting Fragile X syndrome What are the symptoms or characteristics of this disorder or trait? What is the prevalence of the trait or disorder? What are the main genetic factors? s the genetic cause of this disorder or trait known? What gene(s) have been proven to be involved? Or, if not known, what genes are thought to be involved? Is it caused by a single gene? polygenic? Multifactorial? Devote a few paragraphs to this This could be one of the longest parts of the paper, if you choose to focus on this. If multiple genes are thought to be involved, discuss the specific role of at least one of them in depth (if known). Is the gene you’re discussing thought to play a major or a minor role in the phenotype? What chromosome is it on? What protein does it code for, and how might the protein possibly contribute to the phenotype? If no genes have yet been identified, indicate this, and devote at least one paragraph to any current efforts to determine which…
- A young lady requested pre-marital genetic counselling because her sister had died in infancy of gangliosidosis, an autosomal recessive disease. What is the risk that this young lady has similarly affected offspring? What advice should be given?Please summarize and make the following paragraph about treacher collins syndrome disease into important bullet points. Thank you!! A mutation in the TCOF1 gene causes up to 93% of Treacher Collins syndrome cases. This gene, which is found on chromosome 5, is in charge of facial developnent. TCOF1 changes spontaneously in around half of all cases at conception, but no one knows what causes the change. In addition, Treacher Collins syndrome is inherited as an autosomal dominant condition in some cases. This indicates that the child inherits the Treacher Collins syndrome gene from one parent and an unaffected copy from the other. Changes in the POLRIC and POLRID genes may be responsible for another 2% of instances. It's unclear how the mutations in the genes create facial abnormalities. However, during weeks three to eight of embryonic development, they are thought to trigger apoptosis (cell death) of facial bone, cartilage, and soft tissue.Based on the figure below: If children with hereditary retinoblastoma often survive until adulthood and produce children, what is their risk of developing other types of tumors later in life? What is a risk for their children of developing retinoblastoma? Is there the tendency to develop retinoblastoma inherited as a dominant trait or as a recessive trait? Is there one mutant copy sufficient to predispose a person to develop the cancer or two copies are needed to develop retinoblastoma as a cancer?
- Genetic tests that detect mutations in the BRCA1 and BRCA2 oncogenes are widely available. These tests reveal a number of mutations in these genes—mutations that have been linked to familial breast cancer. Assume that a young woman in a suspected breast cancer family takes the BRCA1 and BRCA2 genetic tests and receives negative results. That is, she does not test positive for the mutant alleles of BRCA1 or BRCA2. Can she consider herself free of risk for breast cancer?Part 3C: Below is data from a pedigree trace of patients affected with mouse model of pancreatic cancer, and below are the observations regarding a new gene called 318 that is found on chromosome 5. Patient II-4 has two copies of loss of function variant alleles (or is homozygous for loss-of-function variant 318 allele). Patient I-2 has one copy of loss of function variant and one copy of unaffected allele (is heterozygous for loss-of-function variant 318 allele). Patient II-1 has two copies of unaffected allele (or is homozygous for unaffected 318 allele). |-1 1-2 Il-1 Il-2 Il-3 |l-4 II-5 II-1 III-2 III-3 Based upon data above, what is the mode of inheritance for mouse model for pancreatic cancer? Why?One of the most famous cases of an X-linked recessive mutation in humans is that of hemophilia found in the descendants of Britain’s Queen Victoria. The pedigree of the royal family indicates that Victoria was heterozygous for the trait; however, her father was not affected, and no other member of her maternal line appeared to carry the mutation. What are some possible explanations of how the mutation arose? What types of mutations could lead to the disease?