24. Wild type eye color in Drosophila is brick red due to a mixture of red and brown pigments, which are synthesized through the action of parallel, independent biosynthetic pathways. The X-linked recessive white eye color mutation isolated by T.H. Morgan knocks out both pathways (it affects one gene required for the function of both pathways). Many other eye color mutants have also been isolated, including brown, scarlet, and buff (all of which are recessive). In brown mutants, the red color is missing; in scarlet mutants, the brown color is missing. In the table below, the eye color phenotypes of parents and progeny are given for various crosses carried out with individuals from true-breeding lines (WT stands for wildtype). Note differences in the outcome of reciprocal crosses for some pairwise combinations of mutations. Male and female progeny of each cross had the same eye color phenotypes unless stated. Female Parent → Male Parent ê Brown Scarlet Buff White Brown WT WT WT Scarlet WT WT WT Buff WT Females, White Males WT Females, White Males Buff White WT Females, White Males WT Females, White Males Buff Females, White Males

24. Wild type eye color in Drosophila is brick red due to a mixture of red and brown pigments, which are synthesized through the action of parallel, independent biosynthetic pathways. The X-linked recessive white eye color mutation isolated by T.H. Morgan knocks out both pathways (it affects one gene required for the function of both pathways). Many other eye color mutants have also been isolated, including brown, scarlet, and buff (all of which are recessive). In brown mutants, the red color is missing; in scarlet mutants, the brown color is missing. In the table below, the eye color phenotypes of parents and progeny are given for various crosses carried out with individuals from true-breeding lines (WT stands for wildtype). Note differences in the outcome of reciprocal crosses for some pairwise combinations of mutations. Male and female progeny of each cross had the same eye color phenotypes unless stated. Female Parent → Male Parent ê Brown Scarlet Buff White Brown WT WT WT Scarlet WT WT WT Buff WT Females, White Males WT Females, White Males Buff White WT Females, White Males WT Females, White Males Buff Females, White Males

Biology: The Dynamic Science (MindTap Course List)

4th Edition

ISBN:9781305389892

Author:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Publisher:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Chapter15: From Dna To Protein

Section: Chapter Questions

Problem 15TYK

See similar textbooks

Similar questions

1. a)What would happen if the aminoacyl tRNA synthetase responsible for charging alanine tRNAs also charged methionine tRNAs with alanine? b)What would happen if an individual was homozygous for mutant alleles of the gene encoding the aminoacyl tRNA synthetase responsible for charging leucine tRNAs?
12. a. You want to create a genetic construct that will express GFP in Drosophila. In addition to the GFPcoding sequence, what DNA element(s) must youinclude in order to express this protein in flies if theconstruct were integrated into the Drosophila genome? Where should such DNA element(s) be located? How would you ensure that GFP is expressedonly in certain tissues of the fly, such as the wing?b. Suppose you insert the GFP coding region plus allof the DNA elements required by the answer to part(a)—except the enhancer—between inverted repeatsfound at the ends of a particular transposable element.Because all of the DNA sequences located betweenthese inverted repeats can move from place to placein the Drosophila genome, you can generate manydifferent fly strains, each with the construct integrated at a different genomic location. You now examine animals from each strain for GFPfluorescence. Animals from different strains showdifferent patterns: some glow green in the eyes,others in…
Researchers have exploited Minute mutations in orderto study the phenotypes associated with recessive lethal mutations (l−) that decrease the rate of cell divisionand thus make only very tiny homozygous mutant clones that are difficult to analyze. Many differentstrains of Drosophila carry dominant loss-of-functionMinute (M) mutations in a variety of genes encodingribosomal protein subunits. The M genes are haploinsufficient; flies with only one wild-type M+ gene copyhave a slower pace of cell division, and thus prolongeddevelopment and subtle morphological abnormalities.To circumvent the tiny clone problem, researchersgenerate GFP-marked homozygous l−/ l− clones thatare also M+/ M+, in flies that are l−/ l+ and M−/ M+.The loss of the Minute mutation only in cells withinthe clone gives the l−/ l− cells a growth advantageover their neighbors, enabling the mutant clone togrow large enough to study. Diagram chromosomesthat could be used to generate such clones
8. As explained in the text, the cause of many geneticdiseases cannot yet be discerned by analyzing wholeexome/genome sequences. But in some of theseseemingly intractable cases, important clues can beobtained by looking at mRNAs or proteins, ratherthan at the DNA.a. As you will see in more detail in later chapters, it ispossible to use single-molecule methods to sequence cDNA copies of millions of mRNA molecules from any particular tissue cheaply. Howcould you sometimes use such information to finda disease gene? When would this information benoninformative?b. A technique called Western blotting allows you toexamine any protein for which you have an antibody; it is possible to see differences in size oramount of that protein. How could you sometimesuse such information to find a disease gene? Whenwould this information be noninformative?
2. Null mutations are valuable genetic resources becausethey allow a researcher to determine what happens to anorganism in the complete absence of a particular protein. However, it is often not a trivial matter to determinewhether a mutation represents the null state of the gene.a. Geneticists sometimes use the following test forthe nullness of an allele in a diploid organism: If theabnormal phenotype seen in a homozygote for theallele is identical to that seen in a heterozygote(where one chromosome carries the allele in question and the homologous chromosome is known tobe completely deleted for the gene) then the alleleis null. What is the underlying rationale for thistest? What limitations might there be in interpreting such a result?
Geneticists often use the alkylating agent ethylmethane sulfonate (EMS; see Figure 15.6) 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?
Most organisms display a circadian rhythm, a cycling of biological processes that is roughly synchronized with day length. In Drosophila, pupae eclose (emerge as adults after metamorphosis) at dawn. a)Using this knowledge how would screen for Drosophila mutants that have an impaired circadian rhythm? b)In each case, how would you clone the genes you identified by mutation?
1. How would you determine experimentally mutagenesis caused by stress? 2. What are the evolutionary advantages associated with stress-induced mutagenesis? 3. How do bacteria cope with mutagenesis? List and explain at least three way
Recall that Leber congenital amaurosis (LCA), a formof congenital blindness in humans, can be caused byhomozygosity for recessive mutations in the RPE65gene. Recently, a rare dominant mutation in RPE65has been implicated as one cause of an eye diseasecalled retinitis pigmentosa, which is characterized byretinal degeneration that can progress to blindness.The dominant RPE65 mutation is a missense mutation causing amino acid 447 in the polypeptide tochange from Asp to Glu. Little is known about thenature of the mutant protein.a. Do you think that the dominant allele is morelikely a loss-of-function or a gain-of-functionmutation? Explain.b. As described in this chapter, gene therapy for LCAhas been at least partially successful. Do you thinkthat the same kind of gene therapy can be used forpatients with retinitis pigmentosa caused by thedominant mutant allele of RPE65? Explain.
4 How might transposons be utilized to hereditarily design Drosophila?..
6. Suppose a particular gene is required for early development and also later for development of a particulartissue, such as the adult nervous system. By generating a homozygous mutant clone in that tissue of a heterozygote, researchers can circumvent the lethalitythat would result if the entire animal is homozygousfor a loss-of-function mutation in that gene.A technique called MARCM (Mosaic Analysiswith a Repressible Cell Marker) was developed to enable Drosophila geneticists to generate homozygousmutant cell clones that are marked by the presence of areporter protein such as GFP. Marker expression enables the investigator to observe clearly the mutantphenotype within a clone of mutant cells. This technique relies on a yeast protein called Gal80 that is anegative regulator of the Gal4 protein described previously in Solved Problem II. Gal80 binds to Gal4 andprevents it from activating transcription. The idea ofMARCM is that Gal4/UASG-driven GFP expression isblocked by Gal80 throughout…
Geneticists 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?