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A. Deletion of the SOX9 gene leads to sex reversal resulting in a person with karyotype 46XY being phenotypically Explain the genetic basis for this.
B. Describe what would happen to the
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- Please type your answer 1A. What is the molecular basis for genomic imprinting? B. How is the process of X-chromosome inactivation similar to genomic imprinting. C. How is the process of X-chromosome inactivation different from genomic imprinting. D. In mice, the Igf2 gene inherited from the mother is never expressed in her offspring? Explain. E. What genes are deleted in a female born with Angelman syndrome. Which parent transmitted the deletion to her?Explain why a person with Klinefelter Syndrome (XXY) still exhibits abnormal phenotypes despite the fact that one of the extra X Chromosome is inactivated practically leaving an XY active sex chromosomes similar to a normal male?Explain about how X chromosome inactivation takes place in mammals at the chromosomal and molecular level. B. What genes are involved in inactivating a human X chromosome? . C. What role does X chromosome-specific inactivating transcript --XIST-- non coding RNA play in the inactivation of the human X chromosome.
- Mutations Can Uncouple chromosomal Sex from Phenotypic Sex Discuss whether the following individuals (1) have male or female gonads, (2) are phenotypically male or female (discuss Wolffian/Mllerian ducts and external genitalia), and (3) are sterile or fertile. a. XY, homozygous for a recessive mutation in the testosterone biosynthetic pathway, producing no testosterone b. XX, heterozygous for a dominant mutation in the testosterone biosynthetic pathway, which causes continuous production of testosterone c. XY, heterozygous for a recessive mutation in the MIH gene d. XY, homozygous fora recessive mutation in the SRY gene that abolishes functionColorblindness and hemophilia are both X-linked traits in humans. Explain how a female who has a defective color vision gene on one X chromosome and a defective blood clotting gene causing hemophilia on the other X chromosome can be neither a hemophiliac nor colorblind? Please discuss the effect of Gene dosage compensation in your answer and in your answer describe the molecular process by which this occurs.Give typing answer with explanation and conclusion What characteristics of the DSX protein enable the female- and male-specific isoforms of DSX to regulate the same genes but with different outcomes in female and male development? [multiple answers possible] A.The two isoforms are different alleles of the same gene B.The two isoforms have different DNA-binding domains C.The two isoforms are lncRNAs involved in dosage compensation D.The two isoforms differ in their activation domain E.The two isoforms share the same activation domain F. The two isoforms share the same DNA-binding domain
- In drosophila, a recessive mutation (m-) of a maternal effect gene results in an abnormal phenotype wherein homozygous (m-m-) females produce eggs that cannot support embryonic development. Homozygous (m-m-) males, however, can still produce viable sperm. (A) Using m+ to denote a normal gene, determine the genotypes and phenotypes of the F1s produce by a cross between a heterozygous female and a recessive male. (B) From the offspring, backcross the recessive female with the paternal strain. What are the genotypes and phenotypes of the F2s? (C) If m-m- females produce useless eggs, then how are m-m- produced?Duchenne Muscular Dystrophy (DMD) is a disorder that primarily affects the function of skeletal muscles used for movement and cardiac muscles used for heart beating. Dystrophin is a protein encoded by a single gene, DMD, that is expressed in skeletal and cardiac muscle. Some forms of muscular dystrophy may be caused by different mutations in the DNA sequence of the DMD gene. Because the DMD locus is on the X chromosome, males are affected at higher rates. Two brothers, one of whom has DMD and one of whom does not, worked with their genetic counselor (Links to an external site.) to have their DMD gene sequenced to identify genetic variation that may explain why one brother was affected and the other not. Because DMD is a very long gene, a fictionalized, simplified model of the results is presented here (Figure 1). The actual DMD mRNA is about 16,000 base-pairs!------Consider single nucleotide polymorphism (SNP) #1 (Figure 1). Is this mutation likely to cause Duchenne muscular…Explain why loss-of-function hedgehog and smoothened mutations yield the same phenotype in flies, but a loss-of- function patched mutation yields the opposite phenotype.
- Imagine a scenario in which prenatal testing of a human female fetus indicates that the baby will have a normal XX karyotype but is heterozygous for a mutation that inactivates the Xist promoter. Allele “Xr” represents the mutated version of the Xist promoter, and “XR” represents the normal version of the Xist promoter. How will this mutation affect the process of X inactivation?A. "X inactivation will still be random with both mutant and normal X chromosomes being randomly inactivated" B. "The chromosome with the mutant Xist promoter will always be active" C. "The chromosome with the mutant Xist promoter will always be inactivated" D. "The normal X chromosome (no mutation in Xist) will always be active" E. "The normal X chromosome (no mutation in Xist) will always be inactivated"In drosophila, a recessive mutation (m-) of a maternal effect gene results in an abnormal phenotype wherein homozygous (m-m-) females produce eggs that cannot support embryonic development. Homozygous (m-m-) males, however, can still produce viable sperm. Using m+ to denote a normal gene, determine the genotypes and phenotypes of the F1s produce by a cross between a heterozygous female and a recessive male. From the offspring, backcross the recessive female with the paternal strain. What are the genotypes and phenotypes of the F2s? Show COMPLETE cross for both cases. If m-m- females produce useless eggs, then how are m-m- produced?"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.