Genetic Problems: The Base Sequence On One Strand

Genetic Problems This Is The Base Sequence On One Strand Of A Certa

Identify the complementary DNA strand based on the given DNA sequence; determine the mRNA transcript from the original DNA; deduce the amino acid sequence encoded by the mRNA; analyze the effects of specific mutations on the mRNA and amino acid sequences, including substitutions and insertions; classify the types of mutations; and describe the genetic and phenotypic aspects of sickle cell anemia, along with its relationship to malaria.

Paper For Above instruction

The analysis of genetic sequences and mutations involves understanding the fundamental processes of DNA transcription and translation, as well as the implications of mutations on protein synthesis and disease manifestation. This paper explores these concepts through specific problem scenarios, emphasizing the structure-function relationship of genetic material and its role in health and disease, particularly focusing on sickle cell anemia and its protective effect against malaria.

Part 1: Complementary DNA Strand and mRNA Transcription

The given DNA sequence is 3’ T A C A A T G C C A G T G G T T C G C A C A T T 5’. To determine the complementary DNA strand (the coding strand), we need to find the strand that pairs with the original template strand, adhering to base pairing rules: adenine (A) with thymine (T), thymine (T) with adenine (A), cytosine (C) with guanine (G), and guanine (G) with cytosine (C). Since the original is given in the 3’ to 5’ direction, the complementary strand will be oriented 5’ to 3’. Thus, the complementary DNA strand is 5’ A T G T T A C G G T C A C C A A G C G T G T A A 3’.

Transcription generates mRNA, which mirrors the coding strand (the original DNA strand but with uracil (U) replacing thymine (T)). The mRNA sequence transcribed from the original DNA (template strand) is complementary to the template and identical to the coding strand, except T is replaced by U. Therefore, the mRNA sequence is 5’ A U G U U A C G G U C A C C A A G C G U G U A A 3’.

Part 2: Amino Acid Sequence from mRNA

Using the genetic code, the mRNA sequence is translated into amino acids. The codons are read in groups of three nucleotides starting from the 5’ end. The first codon, AUG, is the start codon, coding for methionine. The subsequent codons code for various amino acids:

  • AUG - Methionine (Start)
  • UUA - Leucine
  • CGG - Arginine
  • CCA - Proline
  • AGC - Serine
  • UGU - Cysteine
  • AAC - Asparagine

Thus, the amino acid sequence is: Methionine-Leucine-Arginine-Tyrosine-Proline-Serine-Cysteine-Asparagine.

Part 3: Effects of Mutations on mRNA and Proteins

Mutation 1: G to C change at the 7th nucleotide of the original DNA

The original nucleotide at position 7 is G. Changing it to C alters the DNA sequence to 3’ T A C A A T C C A G T G G T T C G C A C A T T 5’. Transcription produces the mRNA 5’ A U G U U A G G U C A C C A A G C G U G U A A 3’, with the codons changing accordingly. When translated, the amino acid sequence shifts, and the mutation causes a missense mutation—altering the amino acid sequence and potentially affecting protein function.

Mutation 2: Insertion of G after the 6th nucleotide

Inserting a G after position 6 in the original DNA results in a frameshift mutation, which shifts the reading frame of the mRNA, drastically changing the amino acid sequence downstream of the mutation and often leading to a nonfunctional protein.

Mutation 3: Change at the 11th nucleotide from G to C

This substitution causes another missense mutation, potentially altering protein structure and function, with the specific effects depending on the role of the altered amino acid.

Part 4: Sickle Cell Anemia and Malaria

Sickle cell anemia arises from a point mutation in the gene encoding hemoglobin, specifically a substitution of valine for glutamic acid at the sixth amino acid position of the beta-globin chain. This mutation results from an A to T transversion in the DNA, changing the codon from GAG to GTG in the DNA and from GAG to GUG in mRNA, leading to the incorporation of valine instead of glutamic acid in the hemoglobin protein.

The sickle cell phenotype manifests visibly through misshapen red blood cells that resemble crescents or sickles, contributing to hemolytic anemia, vascular occlusion, and tissue hypoxia. The genotype is typically heterozygous (HbAS), conferring resistance to malaria, especially Plasmodium falciparum, by creating an inhospitable environment for the parasite within the malformed red blood cells. Individuals homozygous for the mutation (HbSS) often suffer from severe anemia and other health issues.

The relationship between sickle cell disease and malaria demonstrates a classic case of balanced polymorphism: the heterozygous state offers a survival advantage in malaria-endemic regions, maintaining the high frequency of the sickle cell allele in such populations despite the deleterious effects in homozygotes.

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