MAKE CONNECTIONS Given that changes in morphologyare often caused by changes in the regulation of geneexpression, predict whether noncoding DNA is likely to beaffected by natural selection. See Concept 18.3 to reviewnoncoding DNA and regulation of gene expression.

MAKE CONNECTIONS Given that changes in morphologyare often caused by changes in the regulation of geneexpression, predict whether noncoding DNA is likely to beaffected by natural selection. See Concept 18.3 to reviewnoncoding DNA and regulation of gene expression.

Name: MAKE CONNECTIONS Given that changes in morphologyare often caused by c
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Description: MAKE CONNECTIONS Given that changes in morphologyare often caused by changes in the regulation of geneexpression, predict whether noncoding DNA is likely to beaffected by natural selection. See Concept 18.3 to reviewnoncoding DNA and regulation of ge

Biology (MindTap Course List)

11th Edition

ISBN:9781337392938

Author:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg

Publisher:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg

Chapter17: Developmental Genetics

Section: Chapter Questions

Problem 13TYU: CONNECT Why is an understanding of gene regulation in eukaryotes crucial to an understanding of...

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For the expression of traits gene provide only the potentialily and the environment provides the opportunity.comment on the statement?
How does position effect influence gene expression? 1 | The movement of the genetic material on the chromosome by inversions or translocations may place a coding sequence near a new regulatory region, thus activating the expression of the gene. The movement of the gene may place it into a region that is highly condensed (heterochromatin). The movement of a gene may remove it from its normal promoter, thus silencing the gene. O All of the above answers are correct
Explain how DNA methylation can regulate gene expression in a tissue-specific way. When and where would de novo methylation occur,and when would demethylation occur? What would occur in the cellsthat give rise to eggs and sperm?
. You receive four strains of yeast in the mail, and theaccompanying instructions state that each strain contains a single copy of transgene A. You grow the fourstrains and determine that only three strains expressthe protein product of transgene A. Further analysisreveals that transgene A is located at a different position in the yeast genome in each of the four strains.Provide a hypothesis to explain this result
I. The retinoic acid receptor (RAR) is a transcription factor that is similar to steroid hormone receptors. Thesubstance (ligand) that binds to this receptor is retinoicacid. One of the genes whose transcription is activatedby retinoic acid binding to the receptor is myoD. Thediagram that follows shows a schematic view of theRAR proteins produced by genes into which one oftwo different 12-base double-stranded oligonucleotides had been inserted in the ORF. The insertion site(a–m) associated with each mutant protein is indicatedwith the appropriate letter on the polypeptide map.For constructs encoding proteins a–e, oligonucleotide 1(5′ TTAATTAATTAA 3′ read off either strand) wasinserted into the RAR gene. For constructs encoding proteins f–m, oligonucleotide 2 (5′ CCGGCCGGCCGG 3′)was inserted into the gene.NH2 f g h i j k l m COOHa b c d eThe wild-type RAR protein can both bind DNA and activate transcription weakly in the absence of retinoic acid(RA) and strongly in RA’s presence. Each…
4e. You also study the expression of 3 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'...TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3' 3' ...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5' * promoter
4e. You also study the expression of 3 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'..TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3’ 3'...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5’ promoter i. Mutant A has a single base pair substitution with the T/A being replaced with C/G base pair at position 35 (position denoted by the * in the sequence above). ii. Mutant B has a 2 G/C pairs inserted between position 19 and 20 (position denoted by the ^ in the sequence above).
concept defines a species as a group of organisms that are capable of exchanging Mayr's genes. O biological species. O cladogenic species O phylogenetic species O evolutionary species O morphospecies Which of the following statements is FALSE? Histone acetylation leads to decreased gene expression. O DNA methylation is associated with epigenetic gene repression. Actually, these are all true statements. O DNA methylation is catalyzed by DNA methyltransferases. Histones can be methylated at lysine residues.
e. You also study the expression of 2 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? o If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'..TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3’ 3' ...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5' promoter i. Mutant A has a single base pair substitution with the T/A being replaced with C/G base pair at position 35 (position denoted by the * in the sequence above).
. Early in development, most human cells turn off expression of an essential component of telomerase, the enzyme responsible for addition of telomere repeat sequences (5’-TTAGGG) to the ends of chromosomes. Thus, as our cells proliferate their telomeres get shorter and shorter, but are normally not lost over the course of a lifetime. If cells are removed from the body and grown in culture, however they ultimately enter a state of replicative senescence and stop dividing when their telomeres get too short. By contrast, most human tumor cells express active telomerase, allowing them to maintain their telomeres and grow beyond the normal limit imposed by senescence - good for them, bad for us. Anticipating a universal cure for cancer, you set up a company to screen chemical ‘libraries’ for telomerase inhibitors. The company share price takes a dive, however, when a rival group generates a strain of telomerase-knockout mice. These mice breed happily for several generations, but…
Researchers have successfully used gene therapy toameliorate some human genetic diseases by adding anormal gene copy to cells whose genomes originallyhad only nonfunctional mutant copies of that gene.For example, a form of blindness due to the lack of asingle protein called RPE65 has been reversed byintroduction of a normal RPE65 gene to cells of theretina of adults.a. The success of this gene therapy approach providesus with clues about the role of the RPE65 proteinin the retina. Do you think that RPE65 is neededfor the proper development of the human eye?b. Can you see a potential difficulty in applying this genetherapy approach for diseases like microcephaly?
6. Suppose a particular gene is required for early development and also later for development of a particulartissue, such as the adult nervous system. By generating a homozygous mutant clone in that tissue of a heterozygote, researchers can circumvent the lethalitythat would result if the entire animal is homozygousfor a loss-of-function mutation in that gene.A technique called MARCM (Mosaic Analysiswith a Repressible Cell Marker) was developed to enable Drosophila geneticists to generate homozygousmutant cell clones that are marked by the presence of areporter protein such as GFP. Marker expression enables the investigator to observe clearly the mutantphenotype within a clone of mutant cells. This technique relies on a yeast protein called Gal80 that is anegative regulator of the Gal4 protein described previously in Solved Problem II. Gal80 binds to Gal4 andprevents it from activating transcription. The idea ofMARCM is that Gal4/UASG-driven GFP expression isblocked by Gal80 throughout…