Standard 2b A male individual who is XYSRY has the following genotype for the AMH gene on chromosome 19: AMH1 AMH2. The AMH1 allele codes for a protein that is capable of binding to the receptor for AMH. The AMH2 allele codes for a protein that is unable to bind with the receptor for AMH. 7. Based on your understanding of biology, what is the likely phenotype of this individual? 8. Create a box-and-arrow model that describes: a. how information in the AMH gene results in the phenotype you identified, above, and b. the origin of the genetic variation in this system. Your model should include the following core structures, contextualize to this case, although you may add or repeat structures as needed: allele, amino acids, gene, nucleotides, phenotype, protein

Standard 2b A male individual who is XYSRY has the following genotype for the AMH gene on chromosome 19: AMH1 AMH2. The AMH1 allele codes for a protein that is capable of binding to the receptor for AMH. The AMH2 allele codes for a protein that is unable to bind with the receptor for AMH. 7. Based on your understanding of biology, what is the likely phenotype of this individual? 8. Create a box-and-arrow model that describes: a. how information in the AMH gene results in the phenotype you identified, above, and b. the origin of the genetic variation in this system. Your model should include the following core structures, contextualize to this case, although you may add or repeat structures as needed: allele, amino acids, gene, nucleotides, phenotype, protein

Name: Standard 2bA male individual who is XYSRY has the following genotype
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Description: Standard 2bA male individual who is XYSRY has the following genotype for the AMH gene on chromosome19: AMH1 AMH2. The AMH1 allele codes for a protein that is capable of binding to the receptorfor AMH. The AMH2 allele codes for a protein that is unab

Biology: The Unity and Diversity of Life (MindTap Course List)

14th Edition

ISBN:9781305073951

Author:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Publisher:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Chapter10: Control Of Gene Expression

Section: Chapter Questions

Problem 3CT: Almost all calico cats (one is pictured in FIGURE 10.7B) are female. Why? B When this calico cat was...

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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?
Colorblindness 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.
In 1952, an article in the British Medical Journalreported interesting differences in the behavior ofblood plasma obtained from several people who suffered from X-linked recessive hemophilia. Whenmixed together, the cell-free blood plasma from certain combinations of individuals could form clots inthe test tube. For example, the following table showswhether clots could form (+) or not (−) in variouscombinations of plasma from four people withhemophilia:1 and 1 − 2 and 3 +1 and 2 − 2 and 4 +1 and 3 + 3 and 3 −1 and 4 + 3 and 4 −2 and 2 − 4 and 4 −What do these data tell you about the inheritance ofhemophilia in these individuals? Do these data allowyou to exclude any models for the biochemical pathway governing blood clotting?
The Xg cell-surface antigen is coded for by a gene located on the X chromosome. No equivalent gene exists on the Y chromosome. Two codominant alleles of this gene have been identified: Xg1 and Xg2. A woman of genotype Xg2/Xg2 bears children with a man of genotype Xg1/Y, and they produce a son with Klinefelter syndrome of genotype Xg1/Xg2Y. Using proper genetic terminology, briefly explain how this individual was generated. In which parent and in which meiotic division did the mistake occur?
. Neurofibromas are tumors of the skin that can arisewhen a skin cell that is originally NF1+/ NF1− losesthe NF1+ allele. This wild-type allele encodes a functional protein (called a tumor suppressor), while theNF1− allele encodes a nonfunctional protein.A patient of genotype NF1+ / NF1− has 20 independent tumors in different areas of the skin. Samplesare taken of normal, noncancerous cells from thispatient, as well as of cells from each of the 20 tumors.Extracts of these samples are analyzed by a techniquecalled gel electrophoresis that can detect variantforms of four different proteins (A, B, C, and D) allencoded by genes that lie on the same autosome asNF1. Each protein has a slow (S) and a fast (F) formthat are encoded by different alleles (for example, ASand AF). In the extract of normal tissue, slow and fastvariants of all four proteins are found. In the extractsof the tumors, 12 had only the fast variants of proteinsA and D but both the fast and slow variants of proteins B and…
Researchers discovered recently that the sole functionof the SRY protein is to activate an autosomal genecalled Sox9 in the presumptive gonad (before it has“decided” to become a testis or an ovary).a. What would be the sex of an XY individual homozygous for nonfunctional mutant alleles of Sox9?Explain.b. Given your answer to part (a), why is SRY, ratherthan Sox9, considered the male determining factor?(Hint: What do you think would happen if you didan experiment like the one in the Fast Forward BoxTransgenic Mice Prove That SRY Is the MalenessFactor, except that you used a Sox9 transgeneinstead of SRY?)
Figure 5.1 presented abbreviated pedigrees looking at the inheritance of X-linked human conditions. El Figure 5.1a initiated with a male who was color blind and had hemophilia A. The grandsons and great-grandsons of this male were either color blind and had hemophilia A, or they had neither condition. a. Which if any individuals in the G Fig. 5.1a pedigree is a double heterozygote? b. Are any of the grandsons or great-grandsons shown in the pedigree the product of recombinant type gametes? c. Do the genes responsible for color blindness and hemophilia A segregate independently? d. If you examined many pedigrees, each starting with a man who was simultaneously color blind and had hemophilia A, do you think any grandsons or great-grandsons would ever have one condition but not the other? L Figure 5.1b initiated with a male who was color blind and had hemophilia B. The grandsons of this male were either only color blind, only had hemophilia B, had both conditions, or they had neither…
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Normal vision (XA) in humans is dominant to color blindness (Xa) and is X-linked. A man with normal vision, whose father was colorblind, marries a colorblind woman. What are the chances that a son will be colorblind? What are the chances that a daughter will be colorblind? The determiner for brown eyes (B) is dominant to blue eyes (b) and is not X-linked. A colorblind man with brown eyes, whose mother was blue-eyed, marries a blue-eyed woman having normal vision, whose father was colorblind. Show the expected phenotypes ratio of their children involving eye color, color blindness, and sex.
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…
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