Answer:
here.
Explanation:
Due to the prevalence of malaria in Africa, the allele for sickle cell anemia (HbS) provides a selective advantage. That's why it remains in the population.
A normal African person (HbAHbA), with normal haemoglobin, will not die of anemia, but will die of malaria.
An African person with sickle cell anemia (HbSHbS), with abnormal haemoglobin, will die of anemia.
A heterozygous African person (HbAHbS), with half of his red blood cells (RBCs) being normal and the other half being sickle-shaped, will neither die from anemia, nor malaria since the plasmodium will be incapable of completing its life cycle in the abnormal RBCs.
Thus heterozygous African people will grow, reproduce and pass on the HbS allele to the next generations.
Must be between G and C. Divide 54 by 2 so we get 27 %.
So, the correct option is '27%'.
Answer:
because they cannot reproduce by themselves without a host viruses are not considered living. Nor do viruses have cells they're very small, much smaller than the cells of living things and are basically just packages of nucleic acid and protein.
Explanation:
Hope this helped Mark BRAINLIEST!!!
Fragmentation or, more correctly, habitat fragmentation is the process of <span><span>modification and </span>division of the habitat of a species. There are mechanisms that lead to
discontinuity in the spatial distribution of resources that affects the occupation, reproduction
and survival of a certain species.
Because of all that there is a strong connection to the welfare and survival of species.</span>
Answer:
Explanation:
A. Cancer cells are cancerous because they divide all the time. Normal cells stop dividing once there's enough of them but cancer cells divide when not required as well. Therefore, if Ras is mutated it will always be "on" which means it will activate the pathway which will lead to division of cells i.e. cells divide to multiply their numbers so more cells will be made. Normally, cells only multiply whne there's the growth factor present to activate the whole pathway, but since Ras is mutated it doesnt need the growth factor to activate the pathway, it automatically always activates the pathway even in absence of growth factor.
B. It is highly unlikely that the proposed drug will have a useful effect. This is because mutant Ras protein of this type behaves as though it is constantly "on". Ras acts downstream of the receptor, i.e. first you have the reception of growth factor in receptor, then the ras gets activated. However, the activating mutation makes its effect felt (Ras is activated no matter if there's a growth factor or not), which is why mutant Ras is always active and no longer dependent on the receptor for activation.
Therefore, blocking the ability of the receptor to dimerize and activate Ras will probably not have an effect on cells containing the mutant Ras protein as it does not inhibit the activity of mutated Ras protein.
(Check out the Ras/Ref/MEK/Erk pathway for better understanding of how significant role Ras protein plays in cell proliferation i.e. division)
