Concept explainers
As described in Chapter 5, not all inherited traits are determined by nuclear genes (i.e., genes located in the cell nucleus) that are expressed during the life of an individual. In particular, maternal effect genes and mitochondrial DNA are notable exceptions. With these ideas in mind, let’s consider the cloning of a sheep (e.g., Dolly).
A. With regard to maternal effect genes, is the
B. Does the cloned animal inherit extranuclear traits from the animal that donated the egg or from the animal that donated the somatic cell? Explain.
C. In what ways would you expect this cloned animal to be similar to or different from the animal that donated the somatic cell? Is it accurate to call such an animal a “clone” of the animal that donated the nucleus?
Want to see the full answer?
Check out a sample textbook solutionChapter 22 Solutions
Genetics: Analysis and Principles
- this is what i have said about this image so far, what else can be said aswell including the raw count column. " Interpreting the results of an RNA-Seq analysis is pivotal in understanding the underlying genetic mechanisms of diseases such as breast cancer. In this analysis, Figure 1 provides comprehensive data on differentially expressed genes associated with breast cancer. By delving into the provided information, we can gain valuable insights into the molecular landscape of this disease. First focus is on the gene with the highest fold change, EYA4, situated on chromosome 6. With a staggering fold change of 3604.4176, EYA4 exhibits an unprecedented level of overexpression in cancerous cells compared to normal cells. This profound alteration suggests a pivotal role for EYA4 in breast cancer pathogenesis. The log2 fold change of 11.81555 further emphasizes the magnitude of this difference in gene expression. Statistical significance is evident, with an exceptionally low p-value of…arrow_forwardresearchers have been able to clonemammals by fusing a cell having a diploid nucleus (i.e., a somaticcell) with an egg that has had its nucleus removed.A. With regard to maternal effect genes, would the phenotype ofsuch a cloned animal be determined by the animal that donatedthe egg or by the animal that donated the somatic cell? Explain.B. Would the cloned animal inherit extranuclear traits from theanimal that donated the egg or from the animal that donated thesomatic cell? Explain.C. In what ways would you expect this cloned animal to be similarto or different from the animal that donated the somatic cell? Isit fair to call such an animal a clone of the animal that donatedthe diploid nucleus?arrow_forwardThe restriction digests of the cloned Drosophila gene can provide direct visible evidence of a mutation, as these samples come from a clone of the gene. In order to similarly detect a mutation in the copy of the endogenous gene within the Drosophila genome, a mechanism for specifically detecting restriction fragments from that gene among the complex set of fragments generated in a restriction digest of the entire Drosophila genome. Remember that the Drosophila melanogaster genome consists of ~123,000 kb. For a 10.2 kb Drosophila gene, what fraction of the genome does this gene constitute?arrow_forward
- The goal of the Knockout Mouse Project is to generate a set of ES cell lines, each with a knockout mutation in a single gene, that collectively contains amutation in every gene in the mouse genome.a. Do you think that it will be possible, for everygene, to generate a heterozygous knockout ES cellline? Explain.b. Do you think that for every heterozygous knockoutES cell line, it will be possible to generate a heterozygous knockout mouse? Explain.c. In fact, investigators failed in their attempts to generate ES cell knockouts for the Fam gene describedin Problem 5. How could these researchers use EScell technology to determine whether Fam is required for eye development in the mouse? Diagrama construct that the researchers could introduceinto ES cells to explore this issue.d. Describe various outcomes that might be obtainedfrom the experiment in part (c) and what you couldconclude in each case.arrow_forwardA normal appearing female infant was identified with a positive newborn screen, linked to chromosome 12. Few years ago, her older sibling had developed profound hypoglycemia, liver failure leading to coma, and subsequent irreparable brain damage, following a viral illness. The sibling was subsequently shown by clinical testing to have the same disorder that this female infant is screened positive for. a. What is the most likely diagnosis? b. What biomarkers would confirm this on the newborn screening process? Describe the mechanism that causes this metabolic defect.arrow_forwardMutations in the HPRT1 gene in humans result in atleast two clinical syndromes. Consult OMIM (www.omim.org) by querying HPRT1; you will only needto look briefly at the top three hits (files #300322,300323, and 308000).a. What is the full name of the HPRT1 enzyme?b. On which chromosome is the HPRT1 gene located?c. Mutations in HPRT1 are associated with two different syndromes. What are these syndromes? Foreach, answer the following questions: (i) What arethe symptoms associated with the syndrome? (ii) Isthe mutant allele that causes the syndrome dominant, recessive, codominant, or incompletely dominant with respect to the normal allele, or do specialconditions apply? (iii) Is the syndrome associatedwith a loss-of-function or a gain-of-function disease allele? (iv) Does the syndrome display allelicheterogeneity? (v) Does the syndrome display locus heterogeneity? (Note: You do not need to understand everything in the OMIM entries to answerthese questions.)arrow_forward
- In the module, you have learned about P-element mediated transgenesis in Drosophila and the concept of using transgenes to rescue mutant phenotypes. In the figure below, you will see a wild type fly with its natural eye colour and three mutants with their eye colours changed to vermillion, white and rosy, respectively. A schematic of P-element mediated transgenesis (as shown in the lectures) is also included in the figure. Please inspect the schematic carefully and choose which of the following statements is true: I. Injection of the white experimental transgene into the vermillion mutant embryo will not change the vermillion mutant phenotype II. Injection of the white experimental transgene in the rosy mutant embryo will change rosy eye colour to red (wild type) III. Injection of the white experimental transgene in the white mutant embryo will not change the white mutant phenotype IV. Injection of the white experimental transgene in the rosy mutant…arrow_forwardIf you wanted to make a mouse model for any of the following human genetic conditions (a–d), indicate which of thefollowing types of mice (i–vi) would be useful to your studies. If more than one answer applies, state which type ofmouse would most successfully mimic the human disease:(i) transgenic mouse overexpressing a normal mouse protein; (ii) transgenic mouse expressing normal amounts of amutant human protein; (iii) transgenic mouse expressing adominant negative form of a protein; (iv) a knockout mouse;(v) a conditional knockout mouse; and (vi) a knockin mousein which the normal allele is replaced with a mutant allelethat is at least partially functional. In all cases, the transgeneor the gene that is knocked out or knocked in is a form of thegene responsible for the disease in question.a. Marfan syndrome (a dominant disease caused byhaploinsufficiency for the FBN1 gene);b. A dominantly inherited autoinflammatory diseasecaused by a hypermorphic missense mutation in thegene PLCG2;c.…arrow_forwardUsing a transgenic technique, propose an experiment to determine whether Cdx2 is sufficient for trophoblast development in the mouse embryo. Describe two results that you would expect to observe at the blastocyst stage if Cdx2 is indeed sufficient for trophoblast development. Be as specific as possible regarding the transgene that you propose for this experiment (including what gene's enhancer you would use in the transgene). Note: you do not need to explain the details of how a transgenic mouse is made. Describe the experiment in steps (Step 1: ..., Step 2: ... etc) and please keep your answer to under 150 words. tips: DONT talk about stop cassetes/memory cassetes, focus on transgenes Paper called "Cdx2 is required for correct cell fate specification and differentiation of trophectoderm in the mouse blastocyst" gave lots of results that you might see,, 6 diff ways that cdx2 is required for trophoblasts need specific gene enhancer (dont just say "expressed enhancer in genital…arrow_forward
- Leber Congenital Amaurosis (LCA) causes progressive vision loss due to defects in the gene that encodes RPE65 isomerase. Affected individuals are homozygous recessive for mutant alleles of the RPE65 gene. You are trying to determine the molecular nature of the mutations in three individuals with LCA. For ease of analysis, you may assume that each individual is homozygous for the same mutant allele (though the three individuals have different mutations than each other). You use the polymerase chain reaction to amplify DNA from each patient and you determine the sequence of the DNA and compare it to unaffected individuals. You identify the following differences. Note that the non-template strand of DNA is given and the changes are highlighted using red boldface. You can assume that the sequences are in the first reading frame (eg. the first three nucleotides of each sequence is a codon). The coding region of the gene is 1602 bp and the position of the sequences shown below is…arrow_forwardIf you wanted to analyze the size and abundance of the HOAP protein in an extract from a Drosophila animal that you think may be mutant for the HOAP gene, what method could you use to target your analysis specifically to the HOAP protein in that extract?arrow_forwardWith the understanding of DNA methylation and gene expression, answer these following questions with as little word as possible. a. What is the difference between a CpG Island vs a CpG-poor region of the genome? b. What is the typical effect of 5mCpG on gene expression, and what two classes of DNA sequences are most heavily methylated? c. What is sex-specific genomic imprinting? Cite at least one example with the given example. d. What is the main function of HOX genes: specifically, the ANT-C vs. the BX-C clusters?arrow_forward
- Human Anatomy & Physiology (11th Edition)BiologyISBN:9780134580999Author:Elaine N. Marieb, Katja N. HoehnPublisher:PEARSONBiology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStaxAnatomy & PhysiologyBiologyISBN:9781259398629Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa StouterPublisher:Mcgraw Hill Education,
- Molecular Biology of the Cell (Sixth Edition)BiologyISBN:9780815344322Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter WalterPublisher:W. W. Norton & CompanyLaboratory Manual For Human Anatomy & PhysiologyBiologyISBN:9781260159363Author:Martin, Terry R., Prentice-craver, CynthiaPublisher:McGraw-Hill Publishing Co.Inquiry Into Life (16th Edition)BiologyISBN:9781260231700Author:Sylvia S. Mader, Michael WindelspechtPublisher:McGraw Hill Education