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a.
To determine:
The consequence of the homozygosity for the null allele of the Abd-B gene in terms of segmental transformations.
Introduction:
The mutation is the change in the
b.
To determine:
The reason due to which segments A5, A6, A7, and A8 are morphologically different.
Introduction:
The homeotic genes that are present in all animals play a significant role in development. These genes are expressed along the anteroposterior axis during the development of the embryo.
c.
To determine:
The segmental transformation that is expected to be seen in an animal that lacks all three genes.
Introduction:
The genes are the sequence of nucleotides that are present on the chromosomes and encode for a specific protein that plays a crucial role in the functioning of the different processes in an organism. The gene is located at specific gene loci and can be structural or regulatory in nature.
d.
To determine:
The nature of the mutations in the Contrabithorax region in terms of dominant or recessive mutations.
Introduction:
A specific class of genes called the segmentation genes function in regulating the formation of specific body structures. In order to form a particular body segment, these segmentation genes collaborate sequentially to determine the destiny of a specified region of the body.
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Chapter 18 Solutions
Genetics: From Genes to Genomes, 5th edition
- The GAL gene system in yeast is used to metabolize galactose. In the presence of galactose, the GAL genes are expressed; however, in the absence of galactose, the GAL genes are repressed. A yeast mutant is discovered that continuously expresses the GAL genes in the presence or absence of galactose. Which one of the following mutations is likely the cause of constitutively expressed GAL genes? deletion of GAL4 deletion of the UAS elements in the regulatory regions of GAL genes O deletion of GAL3 O deletion of GAL80arrow_forwardIn a haploid, a nonsense suppressor su1 acts on mutation1 but not on mutation 2 or 3 of gene P. An unlinked nonsense suppressor su2 works on P mutation 2 but not on 1or 3. Explain this pattern of suppression in regard to thenature of the mutations and the suppressors.arrow_forwardBased on the partial diploid sketched shown in Figure 3, where cross-hatched rectangles and the red bar indicate mutations that inactivate that particular genetic element of the operon, state if expression of Lacl (Lac repressor) and LacZ (Beta-Galactosidase) is (select one of the options below for each genetic element and briefly justify your answer): constitutively ON (in the presence/absence of lactose) constitutively OFF (in the presence/absence of lactose) • inducible by lactose • not enough information given to conclude • none of the above FIGURE 3: lacl laco lacz- lacY lacl laco lacz lacYarrow_forward
- 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.arrow_forwardIn a mutant mouse, it was discovered that a gene "W" is moved from its original chromosomal locus to the telomere region, where chromatin is packed into heterochromatin. Given what we have learned about eukaryotic gene regulation, can you speculate how the expression of gene W in the new mouse line would be changed as compare to the normal mouse? elevated in the mutant mouse than in the wild-type mouse. cannot be determined. O reduced in the mutant mouse than in the wild-type mouse. change in the mutant mouse as compared to the wild-type mouse.arrow_forwardIn humans, dosage compensation is accomplished by: inactivating one X chromosome in female somatic cells inactivating one homolog from each homologous pair of chromosomes in female somatic cells inactivating the Y chromosome in male somatic cells increasing gene expression from the X chromosome in male somatic cellarrow_forward
- The oncogenic protein BETA promotes entry into the S phase of the cell cycle. Phosphorylation of BETA at the amino acid Tyr98 causes BETA to be degraded by the proteasome, thus limiting its abundance. A mutation in the codon encoding Tyr98 changes this residue to Cys, which cannot be phosphorylated. What is the best description of this mutant allele?a) antimorphb) hypermorphc) hypomorphd) amorphe) neomorpharrow_forwardIn tumor cells obtained from patients with Burkittlymphoma, a cancer of the immune system’s B cells,the myc gene often appears close to one of the breakpoints of a reciprocal translocation between chromosomes 8 and 14. In this translocated position, myc is expressed at a higher-than-normal level. Scientists hypothesize that Myc protein overexpression in B cellscontributes to lymphoma formation.a. Explain how transgenic mice produced using pronuclear injection could be used to test this hypothesis. (Assume that you previously cloned a generegulatory region that is active specifically in Bcells throughout the life of the mouse.)b. Suppose you wanted to overexpress Myc only inthe immune cells of mice, starting at one week ofage. To restrict Myc transcription spatially, youwill use same promoter described in part (a). Torestrict Myc transcription temporally, you will usea cre transgene whose expression is controlled byheat shock (hs-cre). Describe the mouse you wouldcreate to accomplish…arrow_forwardCan you please help me by drawing a serie of schematic figures that demonstrates the information in the paragraph below? In addition to phosphorylation, the C-terminal domain of p53 can also be acetylated and sumolated in response to DNA damage. Acetylation and sumolation both result in an increase in the transactivation ability of p53 and may account for this finding. In vivo, IR induces the acetylation of p53 at Lys320 by PCAF and Lys382 by CBP/p300. Acetylation at these sites is dependent on N-terminal phosphorylation at Ser15 and to a lesser extent on phosphorylation at Ser6, Ser9, and Thr18 (Saito et al., 2002; Wahl and Carr, 2001). All of these phosphorylation events are ATM-dependent, although only Ser15 has been shown to be phosphorylated directly by ATM. Sumolation occurs at Lys386 after DNA damage (Muller et al., 2000). Sumolation refers to the covalent attachment of a small ubiquitin-like molecule (SUMO-1) to Lys residues, but in contrast to ubiquitination, does not result…arrow_forward
- Aurora AAurora A is a protein that acts as a kinase (transfers phosphates to molecules). Many types of cancer cells, including breast cancer cells, have higher than normal levels of this protein.Expressions of Aurora A genes in normal breast tissues (n = 10), normal tissues adjacent to tumors (n = 12) and breast tumors (n = 14).Scientists studying the production of Aurora A protein in normal frog cells observed that the amount of this protein in the cells changed throughout the cell cycle.Scientists tested chemicals that block Aurora 2 to see if they could be used as anti-cancer drugs. They found that some of the candidate drugs did slow the growth of cancer cells in cell culture in the lab. But when they tested these drugs in cancer patients to see if the drugs could slow the growth of solid tumors, they found that the benefit to patients was small when compared to the development of severe side effects such as anemia (low red blood cell count) and leukopenia (low white blood cell…arrow_forwardLoss of p53 function occurs in the majority of human tumors. Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function.arrow_forwardIn the Fast Forward Box Visualizing X Chromosome Inactivation in Transgenic Mice, suppose the investigators had looked at the expression of green and red fluorescent protein in early mouse embryos, when the embryos have fewer than 500 cells. What patterns would they likely have observed?arrow_forward
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