Disruption of axonal transport would be a good target for his drug.
<h3>What is disruption of axonal transport?</h3>
- Axonal transport defects are among the early molecular events leading to neurodegeneration in mouse models of amyotrophic lateral sclerosis (ALS).
- Gene expression profiles indicate that dynactin-1 mRNA is downregulated in degenerating spinal motor neurons of autopsied patients with sporadic ALS.
- Disruption of axonal transport also underlies the pathogenesis of spinal muscular atrophy and hereditary spastic paraplegias.
- The neurotoxin β,β′-iminodipropionitrile (IDPN) selectively disrupts slow axonal transport without affecting fast anterograde or retrograde axonal transport.
- Impairment of slow axonal transport causes a proximal accumulation of neurofilaments.
- Because neurofilaments regulate axonal diameter, this accumulation leads to a marked swelling of the axon.
- Acrylamide causes decreased axonal transport, also causing proximal accumulations of neurofilaments and swelling.
To learn more about axonal transport,
brainly.com/question/10600853
#SPJ4
Answer:
Women who carry one copy of the mutated gene still have normal color vision because they have another copy, which is not mutated, in the other X chromosome that will be the dominant one. As a result, the women are carriers of the mutated gene but not color blind.
Explanation:
Colorblindness is a sex-linked mutation. A woman has two X chromosomes, while a man has one X chromosome and one Y chromosome. The mutated gene that causes color blindness is on the X chromosome, and it is OPN1LW. So if a woman has one mutated OPN1LW in one of her two X chromosomes, the OPN1LW gene in the other X chromosome will be the dominant one stopping the woman from being colorblind.
In the case of men, as they only have one X chromosome, if there is a mutation on the OPN1LW in the X chromosome, the men will be colorblind because there is no extra copy of the gene, as it is in women.
#6 is A. They are all composed of one or more cells.
The plants that were allowed to self pollinate were the F1 plants.
The plants that are true breeding are P generation plants.
The plants where there were 3times as many tall plants as short plants are in F2 generation.
<h3><u>Explanation:</u></h3>
This question is based on the Mendel’s Experiment. Sir Gregor Johann Mendel was the father of genetics who experimented on garden pea plants <em>Pisum</em> <em>sativum</em> to see whether the characters got mixed or not and to know the real cause behind different traits of same character in plants.
He took the pure homozygous tall and short plants separately which he called as parental generation or P generation. These plants were homozygous, hence pure breeding.
As these plants were crossed between themselves, then the F1 generation showed all tall plants. This is because of the heterozygous plants which showed character of dominant trait. These plants were allowed to self pollinate.
As a result of self pollination of the F1 plants, the F2 plants were 75% tall in number whereas the other 25% short, which gave the phenotypic ratio of 3:1.
You can draw a free body diagram with two 250N forces acting on the human, one from each side. The net force is 0 because the two applied forces cancel each other out since they are in opposite directions.
