1) Variation: there needs to be a difference in the individuals within a population
2) Inheritance: These variable traits must be able to be passed down genetically
3) Growth rate: There needs to be a growth rate that requires a struggle for resources
4) Survival rate: There needs to be a difference in survival rate for the different variation types... certain variations will live
Answer:
The order must be K2→K1, since the permanently active K1 allele (K1a) is able to propagate the signal onward even when its upstream activator K2 is inactive (K2i). The reverse order would have resulted in a failure to signal (K1a→K2i), since the permanently active K1a kinase would be attempting to activate a dead K2i kinase.
Explanation:
- You characterize a double mutant cell that contains K2 with type I mutation and K1 with type II
mutation.
- You observe that the response is seen even when no extracellular signal is provided.
- In the normal pathway, i f K1 activat es K2, we expect t his combinat ion of two m utants to show no response with or without ext racell ular signal. This is because no matt er how active K1 i s, it would be unable to act ivate a mutant K2 that i s an activit y defi cient. If we reverse the order, K2 activating K1, the above observati on is valid. Therefore, in the normal signaling pathway, K2 activates K1.
Answer:
1. The difference between the normal hemoglobin protein DNA sequence and the sickle cell hemoglobin DNA sequence is a base to base shift, in this case adenine (GAG) to thymine (GTG).
2. The difference affects the amino acid sequence of the protein by replacing glutamic acid (Glu) with valine (Val).
Explanation:
In sickle cell anemia, a change in the DNA nucleotide sequence is observed, where adenine is substituted by thymine, whose expression is the change in the amino acid sequence of globine β, incorporating valine instead of glutamic acid. This represents a molecular mutation - point mutation - by subtitution, which corresponds to missense mutation.
<u>Normal hemoglobin protein in a RBC</u>
DNA CTG ACT CCT GAG GAG AAG TCT
Amino acids Leu Thr Pro Glu Glu Lys Ser
<u>Sickle cell hemoglobin protein in a RBC</u>
DNA CTG ACT CCT <em>GTG</em> GAG AAG TCT
Amino acids Leu Thr Pro <em>Val</em> Glu Lys Ser
When GAG is transcribed to mRNA, the CUC codon is obtained, which codes for glutamic acid. Thymine substitution causes the DNA sequence to change to GTG, which is transcribed as CAC, the codon that encodes the amino acid valine. The <u>change from glutamic acid to valine in β-globin causes an altered hemoglobin, giving the abnormal erythrocytes observed in sickle cell disease</u>.
I think the answer would be 420hg=4,200,000cg
Hi
Do prokaryotic organisms carry out cellular respiration? If so, how?
The answer is yes as well as no, because some prokaryotes like Archeae and some bacteria donot use cellular respiration because they are anaerobic. The Archaea are also known as Methanogens that reduce Carbon di oxide from environment to Methane that is eventually oxidized to NADH (that is used as an energy source).
However, there are some bacteria that use cellular respiration as a source for the energy production.Cellular respiration is a process which occurs in the cells of higher living organisms as well as in cells of some small organisms like Bacteria. During process of cellular respiration in bacteria, glucose is broken down with the help of oxygen into water and Carbon di oxide. In the process of cellular respiration, bacteria just like humans goes through three stepsi.e Glycolysis, Kreb cycle and Electron transport chain that ultimately lead to the production of ATP (energy).
Hope it helps!
