To analyze:
After recognition of an enhancer trap line created by P element transposition in Drosophila in which the marker gene from the enhancer trap is particularly expressed in the wing imaginal disc.
To outline the procedure used to recognize the gene contiguous to the insertion site of the enhancer trap.
To outline the procedure that reveals the expression pattern of the enhancer trap line and reveal the internal gene expression pattern of the contiguous gene.
Introduction:
Enhancer trapping is the method which allows the hijacking of an enhancer from another gene; therefore, it is useful for the identification of the enhancer. This method combines a large number of random insertion mutants with the expression of a reporter gene. The reporter gene is merged with a minimal promoter, which is insufficient to drive a detectable expression of the reporter gene used in the enhancer trapping methods. It utilizes the potential of the genomic enhancer and silencer that lie outside the construction. The expected mutation, induced by transposons, would be the insertional mutation because the additional bases are added to the original gene. The insertion of an additional base pair in the gene sequence leads to the frameshift mutation.
Therefore, the mutagenesis experiment is expected to have either gain-of-function or the loss of function mutation depending on the insertion of a base pair in the transposon. The gain of function would cause overexpression of the gene inserted adjacent to the transposons, in contrast, if it is inserted into the coding region, it would show the loss of function.
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Chapter 15 Solutions
GENETIC ANALYSIS: INTEGRATED - ACCESS
- What would be the most likely effect of inhibiting the translation of hunchback mRNA throughout a Drosophila embryo?arrow_forward(a) Did deletion of any of the possible control elements cause areduction in reporter gene expression? If so, which one(s), and howcan you tell? (b) If loss of a control element causes a reduction ingene expression, what must be the normal role of that controlelement? Provide a biological explanation for how the loss of sucha control element could lead to a reduction in gene expression.arrow_forwardennar region of gene X, which determines the length of the tail in mice, is mutated so that transcription factors bind it at a much higher affinity compared to the wild-type sequence. What is the most likely phenotypic outcome? Tail length will not change because the enhancer is a non-coding sequence Tail length will increased due to increased activity of the gene's promoter Tail length will decreased because any mutation will cause a loss-of-function of these regulatory regions Not just the tail will be enlarged because increased activity of the enhancer will impact many genesarrow_forward
- Suppose expression of gene A is limited to the middle part of the early mouse embryo. Expression of gene B is located on the posterior and anterior ends of the early mouse embryo, but not in the middle. When gene B is mutated, expression of gene A is distributed over the whole embryo. What is a likely explanation for this data? a) Gene A acts as an activator of gene B. Ob) Gene A acts as a repressor of gene B. O c) Gene B acts as an activator of gene A. () d) Gene B acts as a repressor of gene A.arrow_forwardProgesterone is a steroid hormone (also described as a ligand) that prepares the body for pregnancy. It binds to the progesterone receptor (PR) protein in the cytoplasm of various cells. Ligand bound PR acts as a transcriptional activator, binds to the DNA in the promoter region of several genes and leads to transcriptional activation of these genes. Ligand bound PR has been shown to increase the expression of a gene, FKBP5. You are studying the activity of wild-type (WT) and mutant PR in cells by examining expression of FKBP5. Results are obtained as shown in the figure below, where the asterisk indicates when progesterone was (or was not) added to the cells. From the results, which of the following statements can be concluded? WT PR without progesterone WT PR with progesterone Time Time mutant PR without progesterone mutant PR with progesterone Time Time The wild-type PR is unable to increase FKBP5 expression in the absence of ligand The wild-type PR increases FKBP5 expression after…arrow_forwardWhat is the signaling pathway that mediates the organizing activity of the A/P organizer in the Drosophila wing disc? Describe two experiments that suggest this pathway functions to organize pattern and promote growth along the anterior/posterior axis of wing imaginal discs.arrow_forward
- You are working with a fly hair cell developmental system. This Notch/Delta-regulated system results in clusters of cells where the central one differentiates into a specialized hair cell. To better understand this system you have tagged the C-terminal cytoplasmic domain of Notch with GFP. You have done a forward genetic screen to look for mutants that have unusual phenotypes in this Notch system. The first one is a mutation in Notch itself. This mutant is in the ADAM10 cleavage site and blocks proteolysis. Draw the expected outcome for such a mutant: GFP localization and developmental outcome 24hr after differentiation. WT before differentiation WT 24 hours after differentiationarrow_forwardMyoD is a transcriptional activator that turns on theexpression of several muscle-specific genes in humancells. The Id gene product inhibits MyoD action.a. One possibility is that the Id protein directly represses the expression of these muscle-specificgenes. Explain how Id would function if it were arepressor.b. Another possibility is that Id inhibits musclespecific gene transcription indirectly, by preventingMyoD function. Explain how Id could function asan indirect repressor.c. Suppose you know the amino acid sequence ofthe Id protein. How might this information supportthe hypothesis in part (a) or in part (b)?arrow_forwardThe figure below shows 6 genes that are differentially expressed based on their specific enhancers. The different activators (A-F) are proteins that can bind to the appropriate control element in the enhancers of these genes. Use the diagram to answer the following question: What gene(s) would be transcribed if you A, C, E and F enhancers had activators bound to them? No need to explain your answer – just provide the gene(s). ABCD Promoter Brain specific gene ABC F Promoter Liver specific gene C Promoter Heart specific gene A CD Promoter Skin specific gene AB D Promoter Gut specific gene EF Promoter Nose specific genearrow_forward
- The UG4 gene is expressed in the stem and leaf tissue of the plant Arabidopsis thaliana. To identify potential mechanisms regulating UG4 gene expression, six small deletion mutations are made in cloned sequence containing the upstream regulatory region. The full length mutant segments Which mutation(s) affect an enhancer? Why? Which mutations identify the promoter? Why? Speculate about the reason for different transcription rated obtained for fusion constructs E and F.arrow_forwardName the lambda promoters whose expression is regulated by the cro protein. For each promoter you named, is cro an activator or a repressor of transcription from that promoter?arrow_forwardDiscuss the following argument: “if the expression of every gene depends on a set of transcription regulators, then the expression of these regulators must also depend on the expression of other regulators, and their expression must depend on the expression of still other regulators, and so on. cells would therefore need an infinite number of genes, most of which would code for transcription regulators.” how does the cell get by without having to achieve the impossible?arrow_forward
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