Answer:
The tRNA would be unable to read the mRNA CODON, and will be unable to carry its corresponding amino acid
Explanation:
Protein synthesis occurs in two major stages; transcription and translation. Transcription involves the synthesis of a mRNA molecule while translation involves reading the sequence of the mRNA in order to synthesize amino acids that forms protein. Let's look at translation in details. Translation occurs with the help of a type of RNA molecule called transfer RNA (tRNA) present in the RIBOSOME (site of protein synthesis).
The tRNA possesses a group of three nucleotides called ANTICODON, which it uses to read the mRNA codon that is complementary to it i.e. an anticodon UAC will read mRNA codon AUG. The tRNA binds to the mRNA molecule in order to assess its nuceleotide sequence. Once, a complementary anticodon succesfully reads a particular mRNA codon, it carries the amino acid encoded by the mRNA codon it reads to the growing polypeptide chain. This is the normal translation process.
However, as stated in the question, that if a wrong anticidon successfully binds to a codon. This means that the anticodon that binds to the mRNA codon is not complementary to it. What would happen in this case is that the Anticodon will be unable to read that particular codon it binds to because the complementary base pairing rule is used to read i.e. A-U, G-C. Once, the anticodon cannot read the mRNA codon, the tRNA will also be unable to carry the amino acid that is encoded by that CODON.
Answer:
Humans are now responsible for causing changes in the environment that hurt animals and plant species. We take up more space on Earth for our homes and cities. We pollute habitats. We illegally hunt and kill animals. We bring exotic species into habitats. All of these activities take resources and habitats away from plants and animals.
Explanation:
There are different classes of mutation but the descriptions given here are specifically applied to cystic fibrosis, particularly referring to the CFTR (<span>Cystic fibrosis transmembrane conductance regulator) </span>gene.
<u>Mutation Classes</u>
Class I - Gene contains a stop signal that prevents CFTR from being made.
Class II - CFTR is made, but does not reach the cell membrane
Class III - CFTR is made and in the right place, but does not function normally
Class IV - Channel does not move substances efficiently or at all
Class V - <span>CFTR is made in smaller than normal quantities
(Source: </span>https://www.biologycorner.com/worksheets/case_study_cystic_fibrosis.html)
Given these different classes, the easiest one to correct would most likely be Class V, since in this type of mutation, the only problem or abnormality is the production of insufficient amounts of the needed CFTR.
<span>Very very unlikely.
Since the recessive allele is on the X chromosome, in order for a woman to have this condition, both copies of her X chromosome has to have the recessive allele. One copy of the allele would have to come from her mother, and the second copy from her father. The copy from her mother is a 50/50 chance if her mother was heterozygous with one copy of the recessive allele and one copy of a normal allele and therefore didn't exhibit the dystrophy and therefore didn't know she was a carrier. But the father only has 1 copy of the allele and therefore would exhibit the dystrophy and as such would be unlikely to have engaged in procreative sex that would pass on the defective allele to his offspring. This is especially true since duchenne muscular dystrophy will typically start to manifest itself in male children around starting around age 4.</span>