Answer:
The proportions of nucleotides in the newly formed complimentary strand will be:
14% Thymine (T), 33% Adenine (A), 21% Guanine (G), 32% Cytosine (C).
Explanation:
In a double stranded DNA, the nucleotides of one strand binds with nucleotides of another strand through hydrogen bonds.
Adenine binds with thymine by two hydrogen bonds (A=T) and guanine binds with cytosine by three hydrogen bonds (G≡C).
So, the complimentary strand must have
- thymine equal to the amount of adenine in template strand.
- adenine equal to the amount of thymine in template strand.
- guanine equal to the amount of cytosine in template strand.
- cytosine equal to the amount of guanine in template strand.
Answer:
Order the steps to take when drawing electron dot diagrams.
Count the dots to make sure that all of the valence electrons are represented.
✔ 4
Draw dots around the chemical symbol to represent the valence electrons of the atom.
✔ 3
Use the periodic table to find the chemical symbol of the atom and the number of electrons in the valence shell.
✔ 1
Write the chemical symbol of the atom.
✔ 2
Explanation:
I did it on Egde I guess on the answers BTW just to help you guys
Answer:
Brown eyes = 0.5
Blue eyes = 0.5
Explanation:
Given, B ( brown eyes ) is dominant over b ( blue/light eyes ). So,
BB = Brown
Bb = Brown
bb = blue/light
Mr. O'Ryan = blue eyes = bb
Mrs. O'Ryan = heterozygous brown eyes = Bb
Their children: Bb X bb :
B b
b Bb bb
b Bb bb
Half of the children will have Bb genotype and brown eyes, other half will have bb genotype and blue eyes. Hence, Kellan O'Ryan has 0.5 probability of blue eyes and 0.5 probability of brown eyes.
Answer:
PFFT this might help? sorry if not mate
Explanation:
Cell cycle checkpoint controls play a major role in preventing the development of cancer [see Sherr, 1994, for a more detailed discussion]. Major checkpoints occur at the G1 to S phase transition and at the G2 to M phase transitions. Cancer is a genetic disease that arises from defects in growth-promoting oncogenes and growth-suppressing tumor suppressor genes. The p53 tumor suppressor protein plays a role in both the G1/S phase and G2/M phase checkpoints. The mechanism for this activity at the G1/S phase checkpoint is well understood, but its mechanism of action at the G2/M phase checkpoint remains to be elucidated. The p53 protein is thought to prevent chromosomal replication specifically during the cell cycle if DNA damage is present. In addition, p53 can induce a type of programmed cell death, or apoptosis, under certain circumstances. The general goal of p53 appears to be the prevention of cell propagation if mutations are present. The p53 protein acts as a transcription factor by binding to certain specific genes and regulating their expression. One of these, WAF1 or Cip1, is activated by p53 and is an essential downstream mediator of p53-dependent G1/S phase checkpoint control. The function of p53 can be suppressed by another gene, MDM2, which is overexpressed in certain tumorigenic mouse cells and binds to p53 protein, thus inhibiting its transcriptional activation function. Other cellular proteins have been found to bind to p53, but the significance of the associations is not completely understood in all cases. The large number of human cancers in which the p53 gene is altered makes this gene a good candidate for cancer screening approaches.
Answer:
the engineering of rice crops to withstand flooding and contain more nutrients
Explanation:
hope this helps
