Answer:
a. True, b. False, c.True, d. True
Explanation:
a. Base excision repair is started by a DNA glycosylase that recognizes the changes and removes the altered base by cleavage of the glycosidic bond binding the base and the deoxyribose sugar together.
b. Nucleotide excision repair works by a cut-and patch mechanism that removes their heavy lesions, including pyrimidine dimers and nucleotides . Endonucleases are responsible for the lesion of the damaged strand.
c. Nucleotide excision repair is initiated by the proteins namely UvrA, UvrC, and UvrB in Escherichia coli.
-UvrD (helicase II) later removes the damaged strand
-DNA polymerase I (PolI) fills in the resulting gap.
d. DNA glycolases removes the damaged nitrogenous base.
-It leaves the sugar-phosphate backbone intact and thus creating an apurinic/apyrimidinic site, which is commonly referred to as an AP site.
e. Xeroderma pigmentosum complementation group A(XPA)
-This is an essential protein in the nucleotide excision repair pathway.
- It helps to make a pre-incision complex along with other proteins.
Answer:
A
Explanation:
Radioactively labelled amino acids will be found in the ribosomes. These are the organelles that are the site of protein synthesis.
Amino acids are taken up into the cytoplasm from the surrounding cell culture medium. Amino acids are then bound to tRNAs (with the enzyme aminoacyl-tRNA synthetases) and taken to the ribosome, where they are assembled into a polypeptide chain by the translation machinery.
The null hypothesis here is "the insertion of the wild type MSH2 gene does NOT reduce the number of <em>C. neoformans </em>C3 and C6 cells". This hypothesis is not supported by Figure 2, thereby the alternative hypothesis is accepted.
In the scientific method, a null hypothesis is a plausible explanation that states that there is no statistically significant difference between a certain feature and/or variable of a particular population.
In this case, the null hypothesis indicates that there are no differences associated with the insertion of the wild-type MSH2 gene variant (i.e., the normal allele) in the growth rate of <em>C. neoformans</em> strains on a medium containing a toxic chemical (mutagenic agent).
Figure 2 does not support the null hypothesis because the growth of wild-type MSH2 gene inserted <em>C. neoformans</em> C3 and C6 strains is inhibited when they grow on a medium containing a toxic chemical, thereby this hypothesis is rejected and the alternative hypothesis is accepted.
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