Concept explainers
Evidence [see P. G. Shiels, A. J. Kind, K. H. Campbell, et al. (1999), “Analysis of telomere lengths in cloned sheep,” Nature 399, 316–317] suggests that Dolly may have been genetically older than her actual age. As mammals age, the chromosomes in somatic cells tend to shorten from the telomeres. Therefore, older individuals have shorter chromosomes in their somatic cells than do younger ones. When researchers analyzed the chromosomes in the somatic cells of Dolly when she was about 3 years old, the lengths of her chromosomes were consistent with those of a sheep that was significantly older, say, 9–10 years old. (Note: As described in the chapter, the sheep that donated the somatic cell that produced Dolly was 6 years old, and her mammary cells had been grown in culture for several cell doublings before one of the cells was fused with an oocyte.)
A. Suggest an explanation why Dolly’s chromosomes seemed older than they should have been.
B. Let’s suppose that a female sheep (like Dolly), which was produced via reproductive cloning, was mated at age 11 to a normal male sheep and then gave birth to a lamb named Molly. When Molly was 8 years old, a sample of somatic cells was analyzed. How old would you expect Molly’s chromosomes to appear, based on the phenomenon of telomere shortening? Explain your answer.
C. Discuss how the observation of chromosome shortening, which was observed in Dolly, might affect the popularity of reproductive cloning.
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Genetics: Analysis and Principles
- The genome of Drosophila melanogaster, a fruit fly, was sequenced in 2000. However, this “completed” sequence did not include most heterochromatin regions. The heterochromatin was not sequenced until 2007 (R. A. Hoskins et al. 2007. Science 316:1625–1628). Most completed genome sequences do not include heterochromatin. Why is heterochromatin usually not sequenced in genome-sequencing projects?arrow_forwardComparisons between human and chimpanzee genomes indicate that a gene that may function as a wild-type or normal gene in one primate may function as a disease-causing gene in another [The Chimpanzee Sequencing and Analysis Consortium (2005). Nature 437:69–87]. For instance, the PPARG locus (regulator of adipocyte differentiation) is a wild-type allele in chimps but is clearly associated with Type 2 diabetes in humans. What factors might cause this apparent contradiction? Would you consider such apparent contradictions to be rare or common? What impact might such findings have on the use of comparative genomics to identify and design therapies for disease-causing genes in humans?arrow_forwardThe accompanying photo shows a sequencing gel from the original study that first sequenced the cystic fibrosis gene (J. R. Riordan et al. 1989. Science 245:1066–1073). From the photo, determine the sequence of the normal copy of the gene and the sequence of the mutated copy of the gene. Identify the location of the mutation that causes cystic fibrosis. (Hint: The CF mutation is a 3-bp deletion.)arrow_forward
- 1) Do you agree or disagree with this statement? Transposons can cause genomic rearrangements or genomic expansion compared to microsats, which are only associated with genomic expansion. Explain your response. 2) Do you agree or disagree with this statement? Since bone is a non-living structure, it would not be useful for genomic profiling. Explain.arrow_forwardthis 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_forwardWith age, somatic cells are thought to accumulate genomic "scars"as a result of the inaccurate repair of double-strand breaks by non homologous end-joining (NHEJ). Estimates based on the frequency of breaks in primary human fibroblasts suggest that by age 70 each human somatic cell may carry some 2000 NHEJ-induced mutations due to inaccurate repair. If these mutations were distributed randomly around the genome, how many genes would you expect to be affected? Would you expect cell function to be compromised? Why or why not? (Assume that 2% of the genome - 1.5% coding and 0.5% regulatory - is crucial information.)arrow_forward
- . 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…arrow_forwardNorthern blotting, RT-PCR, and microarrays can be used to analyze gene expression. A lab studies yeast cells, comparing their growth in two different sugars, glucose and galactose. One student is comparing expression of the gene HMG2 under these two conditions. Which technique(s) could he use and why? Another student wants to compare expression of all the genes on chromosome 4, of which there are approximately 800. What technique(s) could she use and why?arrow_forwardA group of scientists sequenced the genomes of 12 species of Drosophila (Drosophila 12 Genomes Consortium. 2007. Nature 450:203–218). Data on genome sizes and numbers of protein-encoding genes from this study are given in the accompanying table. Plot the number of protein-encoding genes as a function of genome size for the 12 species of Drosophila. Is there a relation between genome size and number of genes in fruit flies? How does this compare with the relation between genome size and number of genes across all eukaryotes?arrow_forward
- The technique of fluorescence in situ hybridization (FISH) is described. This is another method for examining sequence complexity within a genome. In this method, a DNA sequence, such as a particular gene sequence, can be detected within an intact chromosome by using a DNA probe that is complementary to the sequence.For example, let’s consider the β-globin gene, which isfound on human chromosome 11. A probe complementary to theβ-globin gene binds to that gene and shows up as a brightly colored spot on human chromosome 11. In this way, researchers can detectwhere the β-globin gene is located within a set of chromosomes. Becausethe β-globin gene is unique and because human cells are diploid(i.e., have two copies of each chromosome), a FISH experimentshows two bright spots per cell; the probe binds to each copy ofchromosome 11. What would you expect to see if you used thefollowing types of probes?A. A probe complementary to the Alu sequenceB. A probe complementary to a tandem array near…arrow_forwardAlthough several different mammalian species have been cloned, the efficiency of this process is extremely low. Often tens or even hundreds of oocytes must be implanted with donor nuclei to obtain one healthy live birth. Many researchers believe the difficulties with cloning reside in the epigenetic modifications, such as DNA and histone methylation, that occur within various cells during an individual’s life. How do you suspect such modifications might affect the success of an experimentarrow_forwardGeneticists often use ethylmethane sulfonate (EMS) to induce mutations in Drosophila. Why is EMS a mutagen of choice for genetic research? What would be the effects of EMS in a strain of Drosophila lacking functional mismatch repair systems?arrow_forward
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