Imagine that you could microinject cytochrome cinto the cytosol of wild-type mammalian cells and of cellsthat were doubly defective for Bax and Bak. Would youexpect one, both, or neither type of cell to undergo apopto-sis? Explain your reasoning.
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Imagine that you could microinject cytochrome c
into the cytosol of wild-type mammalian cells and of cells
that were doubly defective for Bax and Bak. Would you
expect one, both, or neither type of cell to undergo apopto-
sis? Explain your reasoning.
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Solved in 2 steps
- It was clear from the early days of studying devel-opment that certain “morphogenetic” substances werepresent in the egg and segregated asymmetrically intocells of the developing embryo. One such investigationin ascidian (sea squirt) embryos examined endodermalalkaline phosphatase, which could be visualized by a his-tochemical stain. Treatment of embryos with cytochalasinB stopped cell division, but did not block expression ofalkaline phosphatase at the appropriate time. Treatmentwith actinomycin D, which blocks transcription, did notinterfere with expression of alkaline phosphatase. Treat-ment with puromycin, which blocks translation, elim-inated expression of alkaline phosphatase. What is thelikely nature of the morphogenetic substance that givesrise to alkaline phosphatase?The Drosophila gene Dscam1 encodes proteins on thesurface of nerve cells (neurons) that govern neuronalconnections. Each neuron has on its surface a singleDscam1 protein of the tens of thousands that exist.The particular Dscam1 protein a neuron expresses isthought to tag the cell uniquely to determine the pathsof the axons and dendrites it will grow. Eukaryoticgenes are monocistronic. How then can a singleDscam1 gene encode tens of thousands of differentproteins?Development of the nematode Caenorhabditis ele-gans generates exactly 959 somatic cells; it also producesan additional 131 cells that are later eliminated by apop-tosis. Classical genetic experiments in C. elegans isolatedmutants that led to the identification of the first genesinvolved in apoptosis. Of the many mutations affectingapoptosis in the nematode, none have ever been found inthe gene for cytochrome c. Why do you suppose that sucha central effector molecule in apoptosis was not found inthe many genetic screens for “death” genes that have beencarried out in C. elegans?
- Hoechst 33342 is a membrane-permeant dye thatfluoresces when it binds to DNA. When a population ofcells is incubated briefly with Hoechst dye and then sortedin a flow cytometer, which measures the fluorescence ofeach cell, the cells display various levels of fluorescence asshown in Figure Q17–1.A mutant haploid strain of Saccharomyces cerevisiae(yeast) called cox2-1 was found that was unable togrow on media containing glycerol as the sole sourceof carbon and energy. (Glycerol is a nonfermentablesubstrate for yeast.) This strain could, however, growon the fermentable substrate glucose. Researchers discovered that cox2-1 cells lack a mitochondrial proteincalled cytochrome c oxidase.a. Explain why cox2-1 cells can grow on mediumcontaining glucose but not on glycerol medium.A mutant haploid strain of Saccharomyces cerevisiae(yeast) called cox2-1 was found that was unable togrow on media containing glycerol as the sole sourceof carbon and energy. (Glycerol is a nonfermentablesubstrate for yeast.) This strain could, however, growon the fermentable substrate glucose. Researchers discovered that cox2-1 cells lack a mitochondrial proteincalled cytochrome c oxidase.a. Explain why cox2-1 cells can grow on mediumcontaining glucose but not on glycerol medium.b. When cox2-1 was crossed with a wild-type yeaststrain and the resultant diploid cells were allowedto grow mitotically, it was found that about half thediploid clones were able to grow on glycerol, whilethe other half could not. The diploid clones thatcould grow on glycerol were induced to sporulate,and they yielded tetrads with four spores that wereall able to grow on glycerol medium. In all of thesetetrads, two of the haploid progeny were of matingtype a and two of mating type α. The diploids thatcould not…
- Mutations in the nuclear laminproteins cause a large number ofdiseases called laminopathies. What dowe not understand about the nuclearlamina that could account for this fact?After a cell "clears" the G₁ restriction checkpoint, it can proceed into S phase. This S phase entry is achieved by a cyclin dependent kinase (Cdk2) and its cyclin (Cyclin E), but additionally requires the action of a protein kinase (CDC2) as well as a phosphatase (CDC25) enzyme. Explain how these 4 proteins work together to orchestrate S phase entry.Mutants of cyclin B that are resistant to degradation by the cyclin B protease have been generated. How would the presence of these cyclin B mutants affect the events at the metaphase to anaphase transition?
- A human gene called theCFTR gene (for cystic fibrosis transmembrane regulator) encodes aprotein that functions in the transport of chloride ions across the cellmembrane. Most people have two copies of a functional CFTR geneand do not have cystic fibrosis. However, a mutant version of the CFTRgene is found in some people. If a person has two mutant copies ofthe gene, he or she develops the disease known as cystic fibrosis. Arethe following descriptions of this disease related to genetics at themolecular, cellular, organism, or population level?A. People with cystic fibrosis have lung problems due to a buildupof thick mucus in their lungs.B. The mutant CFTR gene encodes a defective chloride transporter.C. A defect in the chloride transporter causes a salt imbalance inlung cells.D. Scientists have wondered why the mutant CFTR gene is relativelycommon. In fact, it is the most common mutant gene that causesa severe disease in persons of Northern European descent. Onepossible explanation why…Like Hurler syndrome, Fabry disease involves an abnormal accumulationof substances within lysosomes. However, the lysosomesof individuals with Fabry disease show an abnormal accumulationof lipids. The defective enzyme is α-galactosidase A, which is alysosomal enzyme that functions in lipid metabolism. The enzymaticdefect causes cell damage, especially to the kidneys, heart,and eyes. The gene that encodes α-galactosidase A is found on theX chromosome. Let’s suppose a phenotypically unaffected coupleproduces two sons with Fabry disease and one phenotypicallyunaffected daughter. What is the probability that the daughter willhave an affected son?Explain the mechanism/s through which molecules such as cyanide and rotenone can exert a cytotoxic effect on eukaryotic cells after instances of exposure. In addition describe if you would expect to observe the same phenotype in anaerobic cells or prokaryotic cells after cyanide exposure.