Acetylated chromatin Chromatin FLC FLD FLC 1Acetyl groups on histone proteins destabilize chromatin Transcription Transcription structure. Flowering locus C (FLC) encodes a regulator protein that represses flowering MRNA MRNAI Translation Translation Restoration 5.that removes acetyl of chromatin groups and restores chromatin structure. No transcription Regulator protein Deacetylase 6 No transcription of FC takes place. enzyme No flowering takes place. Flowering locus D (FLD) encodes a deacetylase enzyme.. Flowering is not suppressed, and so flowering takes place. Repression of flowering No repression of flowering 17.3 Flowering in Arabidopsis is controlled in part by FLD, a gene that encodes a deacetylase enzyme.

Acetylated chromatin Chromatin FLC FLD FLC 1Acetyl groups on histone proteins destabilize chromatin Transcription Transcription structure. Flowering locus C (FLC) encodes a regulator protein that represses flowering MRNA MRNAI Translation Translation Restoration 5.that removes acetyl of chromatin groups and restores chromatin structure. No transcription Regulator protein Deacetylase 6 No transcription of FC takes place. enzyme No flowering takes place. Flowering locus D (FLD) encodes a deacetylase enzyme.. Flowering is not suppressed, and so flowering takes place. Repression of flowering No repression of flowering 17.3 Flowering in Arabidopsis is controlled in part by FLD, a gene that encodes a deacetylase enzyme.

Biology: The Unity and Diversity of Life (MindTap Course List)

14th Edition

ISBN:9781305073951

Author:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Publisher:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Chapter31: Animal Tissues And Organ Systems

Section: Chapter Questions

Problem 1CT: IPSCs are nearly identical to human embryonic stem cells in terms of gene expression, but there may...

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Drosophila geneticists have isolated many mutationsthat modify position-effect variegation. Dominantsuppressors of variegation [Su(var)s] cause less frequent inactivation of genes brought near heterochromatin by chromosome rearrangements, whiledominant enhancers of variegation [E(var)s] causemore frequent inactivation of such genes.a. What effects would each of these two kinds of mutations have on position-effect variegation of thewhite gene in Drosophila (that is, would the eyesbe more red or more white)?b. Assuming that these Su(var) and E(var) mutationsare loss-of-function (null) alleles in the corresponding genes, what kinds of proteins do youthink these genes might encode?
Cells go to great length to correctmistakes in the processes of DNAreplication, transcription, splicing,and translation. Are there analogousstrategies to correct mistakes in theselection of which genes are to beexpressed in a given cell type? Couldthe great complexity of transcriptioninitiation in animals and plants reflectsuch a strategy?
When the DNA of a human cell becomes damaged, the p53 geneis activated. What is the general function of the p53 protein?Is it an enzyme, transcription factor, cell-cycle protein, orsomething else? Describe three ways in which the synthesisof the p53 protein affects cellular function. Why is it beneficialfor these three things to happen when a cell’s DNA hasbeen damaged?
IPSCs are nearly identical to human embryonic stem cells in terms of gene expression, but there may be other ways in which they are not equivalent. For example, the telomeres of IPSCs often vary in length, with many IPSCs cells having telomeres shorter than those of embryonic. How might shortened telomeres affect the life-span of IPSCs or of differentiated cells derived from them?
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?
Look at the two yeast colonies in Figure Q4–3. Eachof these colonies contains about 100,000 cells descendedfrom a single yeast cell, originally somewhere in the mid-dle of the clump. A white colony arises when the Ade2 geneis expressed from its normal chromosomal location. Whenthe Ade2 gene is moved to a location near a telomere, itis packed into heterochromatin and inactivated in mostcells, giving rise to colonies that are mostly red. In theselargely red colonies, white sectors fan out from the middleof the colony. In both the red and white sectors, the Ade2 gene is still located near telomeres. Explain why white sec-tors have formed near the rim of the red colony. Based onthe patterns observed, what can you conclude about thepropagation of the transcriptional state of the Ade2 genefrom mother to daughter cells in this experiment?
The chromosome 9/22 translocation associated withCML (chronic myelogenous leukemia) is called thePhiladelphia chromosome after the city in which itscancer association was first discovered in 1960.People with CML do not inherit this translocation—it occurs in somatic cells. Why do you think that thisparticular translocation that fuses the bcr and ablgenes happens independently in the somatic cellsof many different people?
In contrast to their similar brain abnormalities,newborn mice deficient in Apaf1 or caspase-9 have dis-tinctive abnormalities in their paws. Apaf1-deficient micefail to eliminate the webs between their developing digits,whereas caspase-9-deficient mice have normally formeddigits (Figure Q18–1). If Apaf1 and caspase-9 function inthe same apoptotic pathway, how is it possible for thesedeficient mice to differ in web-cell apoptosis?
Give at least one example of a chromosomal structureor function affected by the following mechanisms formodulating chromatin structure:a. Posttranslational changes of the normal histonesfound in the nucleosome
A cloned gene fragment contains a regulatory element that isrecognized by a regulatory transcription factor. Previousexperiments have shown that the presence of a hormone resultsin transcriptional activation by this transcription factor. To studythis effect, you conduct an electrophoretic mobility shift assayand obtain the following results: Explain the action of the hormone.
Melanosomes are specialized lysosomes that storepigments for eventual release by exocytosis. Various cellssuch as skin and hair cells then take up the pigment, whichaccounts for their characteristic pigmentation. Mousemutants that have defective melanosomes often have paleor unusual coat colors. One such light-colored mouse, theMocha mouse (Figure Q13–3), has a defect in the gene forone of the subunits of the adaptor protein complex AP3,which is associated with coated vesicles budding from thetrans Golgi network. How might the loss of AP3 cause adefect in melanosomes?
Researchers know that Fru-M controls male sexualbehavior in Drosophila because inappropriate Fru-Mexpression in females causes them to behave likemales: Such females display male behaviors that areoriented toward other females.a. Describe a fru mutation that could cause the expression of Fru-M in females.b. Describe a transgene construct that scientistscould generate and insert into Drosophila femalesthat would have the same effect as the mutant youdescribed in (a).