Answer:
Semi-conservative replication is meant for the description of DNA replication and it i s called so because parent DNA helix produces two copies of original DNA, one of which consist of original DNA.
The three main steps in DNA replication includes Initiation, Elongation and Termination.
In the initiation phase, replication begins at origin of replication where helicase enzyme breaks the hydrogen bonds between base pairs and tends to unwind the double helix where the topoisomerase stabilizes the newly formed single strand DNA. DNA polymerase allows elongation to occur in leading direction and catalyses the addition of new nucleotide to new single strands. short sequences of RNA called primers paired to template strands with the help of primase. replication of both strands occurs at the same time one in continuous (3'-5') and other in discontinuous (5'-3') direction, which are called leading strands. new nucleotides added in 3' end and moving to replication fork while discontinuous synthesis occur on parent strand (5'-3') called lagging strand and completed in segments called okazaki fragments. Then primase add primers ahead at 5' end of the lagging strand. DNA polymerase ||| adds short sequences of nucleotides to the primer. During termination, exonuclease replaces DNA primer and DNA nucleotide and DNA ligase helps in making bonding between fragments and replaced nucleotide. Another exonuclease helps in proofreading the newly formed DNA and corrects the errors in sequences. At the end of the parent strands, telomeres are present which keeps on catalyzing by telomerase and completes, the formation of copies of parent DNA.
I don’t know how to explain it but this might help
Answer:
nucleus,chloroplast,cell wall, cell membrane
Explanation:
He demonstrated that SCD and sickle cell trait were due to the presence of abnormal 8-globin polypeptides in red blood cells. He demonstrated that the electrophhoretic mobility of B-globin from patients with SCD was different from that of healthy individuals. He demonstrated that both parents of multiple patients with SCD had low levels of sickled red blood cells. He hypothesized that SCD was a recessive trait and that the parents of patients with SCD would be heterozygous carriers. He demonstrated that the difference between B-globin polypeptides in individuals who were healthy and those with SCD is an amino acid substitution. He performed a peptide fingerprint analysis on B-globin from individuals with 84 84 and 89 88, which identified the segment of B-globin that was changed by the BS mutation. James Neel Linus Pauling Vernon Ingram
hope it helps..
