Answer:
B. option A 2 daughter cells
C. option D metaphase
Answer:
C. Beak size is an inherited trait in the finch population under study.
D. Birds that could eat larger, tougher seeds survived and reproduced during the drought.
E. Beak size varies among the birds in the finch population under study.
Explanation:
The presence of genetic variations among the individuals of a population is required for natural selection to be operative. Natural selection targets the beneficial genetic variations present in the population. Natural selection refers to the differential reproductive and survival success of organisms of a population due to some beneficial genetic traits. These organisms with beneficial genetic traits are able to survive and leave more progeny under prevailing conditions.
If the natural selection has occurred in the ground finch population for the beak size, the beak size should be a genetic trait since natural selection works on genetic traits only. The finch population should have variations with respect to the beak size. The finches having the larger beak size that enabled them to feed on larger, tougher seeds should have higher survival and reproductive fitness during the drought.
Under these conditions, natural selection would favor the finches with larger beak size and would eventually result in an increase in the average beak size of the future generations.
<h2>CRISPR/Cas9</h2>
Explanation:
CRISPR can be used to reintroduce dystrophin back into the KO mouse
- CRISPR stands for Clustered Regularly Interspaced Short Palindromic Repeats and is used to for gene editing
- CRISPR/Cas-mediated genome editing has been shown to permanently correct DMD mutations and restore dystrophin function in mouse models
- Germline editing by injecting zygotes with CRISPR/Cas9 editing component was first done in mdx mice by correcting the mutated exon 23
- Postnatal editing of mdx mice was then achieved using recombinant adeno-associated virus to deliver CRISPR/Cas9 genome editing components and correct the dystrophin gene by skipping or deleting the mutated exon 23 in vivo
- Germline and postnatal CRISPR/Cas9 editing approaches both successfully restored dystrophin function in the mice and same technique can be used for KO mouse model