In this problem we will explore some of the many ways that mutations in two different genes can interact to produce different Mendelian ratios. Consider a hypothetical insect species that has red eyes. Imagine mutations in two different unlinked genes that can, in certain combinations, block the formation of red eye pigment yielding mutants with white eyes. In principle, there are two different possible arrangements for two biochemical steps responsible for the formation of red eye pigment. The two genes might act in series such that a mutation in either gene would block the formation of red pigment. Alternatively, the two genes could act in parallel such that mutations in both genes would be required to block the formation of red pigment.

Further complexity arises from the possibility that mutations in either gene that lead to a block in enzymatic activity could be either dominant or recessive. If the crosses is made between a wild type insect with red eyes and a true breeding white eyed strain with mutations in both genes. Such considerations yield the Pathways in series with recessive mutations in both genes, the F1 progeny shows will have red eye, what is the expected phenotypic ratio of red to white eyed insects in the F2.

#Question id: 1522

#Unit 4. Cell Communication and Cell Signaling

Conversion of a proto-oncogene into an oncogene, also called activation, generally involves a gain-of-function mutation. Following statements are regarding to the mechanisms that produce oncogenes from the corresponding proto-oncogenes.

A. A change in a single base pair in a proto-oncogene that results in a hyperactive or constitutively active protein product.

B. A chromosomal translocation that fuses two genes together to produce a hybrid gene encoding a chimeric protein whose activity, unlike that of the parent proteins, is permanently suppress.

C. A chromosomal translocation that brings a growth regulatory gene under the control of alternative enhancers that cause inappropriate expression of the gene.

D. Amplification of a DNA segment including a proto-oncogene so that numerous copies exist, leading to overproduction of the encoded protein.

Which of the following statements are correct?

#Question id: 1521

#Unit 4. Cell Communication and Cell Signaling

we examine how the deregulation of growth-promoting and growth-inhibiting signaling pathways contributes to tumorigenesis. Mutations-

A. A mutation that alters a single amino acid (valine to glutamine) in the transmembrane region of the HER2 receptor

B. A deletion that causes loss of the extracellular ligand-binding domain in the EGF receptor Results-

i. dimerization of the receptor, even in the absence of the normal EGF-related ligand, transforming it into the oncoprotein, a constitutively active kinase

ii. to constitutive activation of the kinase activity of the resulting oncoprotein

iii. no dimerization, even in the presence of the normal EGF-related ligand, repression of kinase activity

which of the following results are displayed after these mutations?

#Question id: 1520

#Unit 4. Cell Communication and Cell Signaling

Following statements are regarding to enzymatic processing of benzo(a)pyrene to a more potent mutagen and carcinogen.

A. Liver enzymes, particularly P-450 enzymes, modify benzo(a)pyrene in a series of reactions, producing 7,8-diol-9,10-epoxide, a highly potent mutagenic species that reacts with DNA primarily at the N2 atom of a guanine base.

B. The adduct, (+)-trans-anti-B(a)P-N2-dG, causes polymerase to insert an A rather than a C opposite the modified G base. Next time the DNA is replicated, a T will be inserted opposite the A, and the mutation will be complete.

C. Potent mutagen majorly causes conversion of guanine (G) to thymine (T) bases, a transition mutation.

D. When this potent mutagen applied to cultured bronchial epithelial cells, activated benzo(a)pyrene induces many mutations, including activating mutations at codons 175, 248, and 273 of the p53 gene.

Which of the following statements are correct?

#Question id: 1519

#Unit 4. Cell Communication and Cell Signaling

Following statements are regarding to the FOXO3a protein.

A. In the presence of growth factors, FOXO3a is non phosphorylated and mainly localizes to the nucleus, where it activates transcription of several genes encoding pro-apoptotic proteins.

B. When growth factors are removed from the cells, PKB becomes active and phosphorylates FOXO3a.

C. Phosphorylated FOXO3a binds to cytosolic phosphoserine-binding protein 14-3-3 to bind FOXO3a and thus sequester it in the cytosol.

D. Dephosphorylated FOXO3a binds to cytosolic phosphoserine-binding protein 14-3-3 to bind FOXO3a and thus sequester it in the cytosol.

Which of the following is correct?

#Question id: 1518

#Unit 4. Cell Communication and Cell Signaling

Following statements are regarding to the some cancers harbor characteristic chromosome alterations. Chronic myelogenous leukemia (CML), a common leukemia in humans, was found to be associated with the Philadelphia chromosome.

A. Philadelphia chromosome is generated by a translocation between chromosomes 22 and 9. The two chromosomes exchange their terminal regions, which leads to a characteristic alteration in the size of chromosome 9.

B. At the breakpoint of this translocation, a new fusion protein, the BCR-ABL fusion, is generated.

C. The BCR-ABL fusion protein is a constitutively active kinase that phosphorylates multiple signal-transducing proteins.

D. If this translocation occurs in a hematopoietic cell in the bone marrow, the activity of the chimeric BCR-ABL oncogene dephosphorylate proteins thereby activating many intracellular signal-transducing proteins.

Which of the following statements are incorrect?

#Question id: 1263

#Unit 4. Cell Communication and Cell Signaling

The major classes of CAMs include

a. cadherins.    b. fibronectin.    c. Ig-superfamily CAMs.      d. P-selectins.