BIOL 241 Exam 3

You have isolated three different Drosophila recessive mutants (1, 2, and 3) that disrupt the formation of R7 photoreceptor cells during eye formation. To ask in which cell is the gene product required, mosaic analysis were performed for all three mutations and the results are shown below. For each mutation, the open cells represent homozygous mutant cells, whereas the filled cells represent the wild type cells. Based on these please answer the following questions: Mutant 3: 2-3-8 3-4-5 2-5-6-7 2-7 1-8 2-7-8 for mutant 3, which cells is the responsible gene is required in? (Enter 1, 2, 3, 4, 5, 6, 7, or 8)

2

You have isolated three different Drosophila recessive mutants (1, 2, and 3) that disrupt the formation of R7 photoreceptor cells during eye formation. To ask in which cell is the gene product required, mosaic analysis were performed for all three mutations and the results are shown below. For each mutation, the open cells represent homozygous mutant cells, whereas the filled cells represent the wild type cells. Based on these please answer the following questions: Mutant 1: 2-3-8 3-4-5-7 2-5-6-7 7-8 1-7-8 1-7-8 For mutant 1, which cells is the responsible gene is required in? (Enter 1, 2, 3, 4, 5, 6, 7, or 8)

7

You have isolated three different Drosophila recessive mutants (1, 2, and 3) that disrupt the formation of R7 photoreceptor cells during eye formation. To ask in which cell is the gene product required, mosaic analysis were performed for all three mutations and the results are shown below. For each mutation, the open cells represent homozygous mutant cells, whereas the filled cells represent the wild type cells. Based on these please answer the following questions: Mutant 2: 2-4 3-5 2-5-6-7-8 7-8 1-8 2-7-8 for mutant 2, which cells is the responsible gene is required in? (Enter 1, 2, 3, 4, 5, 6, 7, or 8)

8

Regarding Drosophila bicoid, which of the following statements is incorrect? A) The localization determinant for bicoid mRNA is in 5'UTR. B) Bicoid gene encodes a homeodomain-containing transcription factor. C) Bicoid controls the formation of anterior structures. D) Bicoid is a maternal-effect gene. E) Bicoid acts as a morphogen.

A) The localization determinant for bicoid mRNA is in 5'UTR. **3'UTR is the determinant of localization

You have isolated a mutant affecting anterior-posterior patterning of the Drosophila embryo, in which every other segment of the developing mutant embryo was missing. Based on this observation, the mutation is likely be in a A) Pair-rule gene B) Gap gene C) Homeotic gene D) Segmental polarity gene E) Maternal-effect cardinal gene

A) pair-rule gene

Many of oncogenic mutations are dominant. Which of the following general types of mutations have the potential to create dominant oncogenes? A) a nonsense mutation located shortly after the beginning of translation in a gene that encodes a growth-factor receptor. B) a mutation in E2F that disrupts its ability to bind RB C) a mutation that decreases the function of a transcriptional activator of cyclin A. D) a mutation that disrupts the active site of a cytoplasmic tyrosine-specific protein kinase. E) a mutation that keep Ras in the GDP-bound state.

B) a mutation in E2F that disrupts its ability to bind RB

Which of the following genes is known as "the guardian of the genome"? A) Cyclin-dependent kinase B) p53 C) Cyclin D) E2F E) pRB

B) p53

We have learned about the C. elegans pathways required for proper vulva development in lecture. Based on our discussion, please answer the following questions. What will the phenotype be, if the anchor cell is ablated? A) normal B) multivulva C) vulvaless

C) vulvaless if there is no Anchor cell, then no vulva development occurs

Regarding Hox genes, which of the following statements is incorrect? A)The arrangement of Hox genes on chromosome is co-linear with structures specified by these genes. B)The organization and function of Hox genes are conserved in mammals. C)In Drosophila Hox mutants, the number of segments is affected. D)Drosophila contains two Hox gene complexes. E) Hox genes encode transcription factors, which include DNA-binding homeodomain.

C)In Drosophila Hox mutants, the number of segments is affected. **the number of segments remains the same!

Which of the following statements is true regarding the generation of antibody diversity? A) The diversity is generated by RNA-mediated gene silencing. B)The diversity is generated by exon shuffling. C)The diversity is generated by gene rearrangement in both the immunoglobulin heavy chain and light chain loci. D)The diversity is generated by alternative splicing in both the immunoglobulin heavy chain and light chain loci. E)The diversity is generated by gene rearrangement only in the immunoglobulin heavy chain locus.

C)The diversity is generated by gene rearrangement in both the immunoglobulin heavy chain and light chain loci.

You have cloned a piece of DNA that contains the candidate gene. In situ hybridization using this DNA was performed to determine the expression pattern of this gene during embryogenesis. Based on the discussion in class, you'll expect to see A) broad stripes that span several segments B) Gradient concentrated in either anterior or posterior pole C) 14 stripes D) 7 stripes

D) 7 stripes

In Saccharomyces cerevisiae, a cross between a haploid suppressive petite mutant and a haploid wild type results in petite diploid progeny. This is because A) The petite mutant contains a dominant negative mutation in a nuclear gene, which is required for mitochondria function. B) The petite mutant contains extensive deletion in mtDNA, which renders the mitochondria non-functional. C) The petite mutant contains a loss-of-function mutation in nuclear gene, which is required for mitochondria function. D) The petite mutant contains deletion in mtDNA, which give nonfunctional mutant mitochondria proliferation advantage. E) The petite mutant has a diploid mitochondria genome.

D) The petite mutant contains deletion in mtDNA, which give nonfunctional mutant mitochondria proliferation advantage.

The transmission of prion is sensitive to the treatment of: a) dideoxy nucleotides B) RNase C) DNase D) Protease E) UV light

D) protease

During Drosophila eye development, the R7 photoreceptor is specified by the activation of Sevenless (Sev) receptor tyrosine kinase. Sev is activated by Bride-of-sevenless (Boss) ligand, which is expressed on the surface of R8 photoreceptor cell. Once bound by Boss, Sev activates the Ras/MAP kinase cascade to regulate cell fate. As expected, animals mutant for Sev or Boss lack R7 photoreceptors. In wild type, multiple cells express Sev but only one becomes R7 because only one of these Sev-expressing cells contacts the Boss-expressing R8. However, some of these Sev-expressing cells have the potential to become R7 cells if the Sev cascade is activated. For example, expression of constitutively active Sev receptor tyrosine kinase or RasV12 (GTP-bound form) in these cells will generate multiple R7 cells. Base on these information, predict the phenotype of a fly that is sev- but expresses RasV12 in these R7 precursor cells.

Multiple R7 cells b/c RasV12 locks Ras to be active, so the cascade is already activated (meaning there is no need for sev)

During Drosophila eye development, the R7 photoreceptor is specified by the activation of Sevenless (Sev) receptor tyrosine kinase. Sev is activated by Bride-of-sevenless (Boss) ligand, which is expressed on the surface of R8 photoreceptor cell. Once bound by Boss, Sev activates the Ras/MAP kinase cascade to regulate cell fate. As expected, animals mutant for Sev or Boss lack R7 photoreceptors. In wild type, multiple cells express Sev but only one becomes R7 because only one of these Sev-expressing cells contacts the Boss-expressing R8. However, some of these Sev-expressing cells have the potential to become R7 cells if the Sev cascade is activated. For example, expression of constitutively active Sev receptor tyrosine kinase or RasV12 (GTP-bound form) in these cells will generate multiple R7 cells. Predict the phenotype of a fly that is sev- but expresses Boss ectopically (Boss is expressed everywhere)

No R7 cells b/c without sev, Boss does nothing

The maternal-effect mutation torso (tor) is recessive. In the absence of the torso protein product, embryogenesis is not completed (missing both head and tail structures). Consider a cross between a female heterozygous for the torso (tor+/tor-) and a male homozygous for the mutation (tor-/tor-). What will the phenotype(s) of the progeny be?

all are normal

Suppose you have the capability to mutate the GAP (GTPase activating protein) genes in the erbB-expressing cells, will this enhance or suppress the ability of erbB to promote tumor progression?

enhance

We have learned about the C. elegans pathways required for proper vulva development in lecture. Based on our discussion, please answer the following questions. What is the expected phenotype if you overexpress lin-3?

multivulva

We have learned about the C. elegans pathways required for proper vulva development in lecture. Based on our discussion, please answer the following questions. What is the expected phenotype if you express a mutant let-60 with a mutation analogous to those of oncogenic Ras (let-60 is the worm ortholog of Ras)?

multivulva *note: oncogenic Ras mutation causes Ras to be permanently switched "ON" *Ras genes encode signal transduction molecules that regulate cell growth and division *mutated Ras cause overactive signaling

The oncogene erbB is a constitutively active form of a receptor tyrosine kinase that sends unregulated signals, from the plasma membrane, to stimulate cell proliferation. Suppose you have the capability to mutate all the copies of Ras genes in these erbB-expressing cells, will this enhance or suppress the ability of erbB to promote tumor progression?

supress

To analyze the genes required for C. elegans vulva development, you have made an animal mosaic for lin-3. Please predict the phenotype of the mosaic animal if the anchor cell is lin-3[-] and the vulva precursor cells (e.g. P5.p, P6.p, and P7.p) are wild-type.

vulvaless

We have learned about the C. elegans pathways required for proper vulva development in lecture. Based on our discussion, please answer the following questions. What is the expected phenotype of loss-of-function lin-3?

vulvaless lin-3 function is required in the anchor cell for pnp to become vulva cells

In a different mosaic animal, the anchor cells is wild-type, and the vulva precursor cells are lin-3[-]. What will be the phenotype of this mosaic animal?

wild type (lin-3 is only necessary for Anchor cell) *lin-23 function required for pnp cells