A (virtual) place for BIOL335 (2008) people to ask questions, answer questions, make requests, comment, wonder, discuss, complain and rejoice.
Monday, April 14, 2008
Q&As
Please check the link to our answers to practice questions regularly...I am posting Q&As that I got by email.
14 comments:
Anonymous
said...
Is there any extra gene cloning question that I can work on? I have encountered many, and everytime I never get perfect answer by myself. Once i get the answer, everything seems very logic, it's just so hard to get there. So Pam, im just wondering if you could post any good question regarding to gene cloning (functional, positional) with the answer=) Thanks!
sorry...I don't recall that there was a practice midterm posted on the biol 335 website before. does anyone know if it is still there...cause I can't seem to find the link to it..
Just wondering for Q6b regarding the development questions by Dr.H., shouldn't the answer be that Hb will always be an activator? rather than a inhibitor.
Hi Pam. I am a little confused on what we are suppose to know about Su(var) genes. Are we suppose to know the techniques on how the identified them or just know what Su(var) genes do in general?
For the FCD pedigree-molecular markers question, why doesn't the uncle with the het morph have the disease, since the disease is dominant and ppl with the disease in the family should have the same morph right?
For Dr Haughn's questions: hb can act as an inhibitor or as an activator. For example, if it binds to H2, then it will prevent bcd from binding to B1, so it will effectively act as an inhibitor
I assume you are talking about individual 3 in generation II. he does not have the disease, so he must have received his "high band" from his dad (who does not have the disease either) and his "low bands" from his mom, who has the disease allele on the chromosome that has the "high band".
The mom and dad of II-3 (people 1 and 2 in generation I) are actually coming from two distinct families: in the dad's family there is no disease, but people still have the polymorphisms!
Hi Pam, I was just doing one of the problems you gave us about swapping the 3' UTRs of bcd and nos and how that would affect the phenotype the embryo of a female homozygous mutant for bcd and nos and carries both swap constructs... I have written down that they would have "no nos and no bcd".. but I'm not sure if this is correct. If it is, why? and If it's not.. what's the correct answer??
Just want to clarify, isn't the FCD on the mother carried on the "low band"? Since the "low band" homozygous sister (II2) has inherited the disease while the "high band" homozygous sister (II1) do not have the disease.
So II3 do not have the disease becase he received his "low band" from dad and "high band" from mom, both of which are not linked to the FCD allele. While II4 received his "high band" from dad and "low band" from mom (which carries the domiant FCD allele).
One thing I am still confused about this question is that, if this disease is dominant, then how come it is still "rare"? Since only one copy of its allele is required for phenotypical expression, meaning that 50% of progeny between a cross of heterozygous (FCD/fcd) parent and homozygous (fcd/fcd) parent will have this disease, which is quite a high ratio.
the fact that an allele is rare does not mean it can't be dominant! It just means that it's an allele that very, very few people have in the whole population. It is an important piece of information to know when we solve pedigrees, because it allows us to assume that all the people who "marry in" into a family are homozygous for the frequent allele-unless there is direct evidence for the contrary.
(the first question on the sheet that had 2 questions)
--> The embryo does not have bcd or nos OF ITS OWN, or FROM ITS OWN MOM. The only bcd and nos that it has, are the ones with the swapped 3'UTRs. That's what your notes meant, I assume.
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14 comments:
Is there any extra gene cloning question that I can work on? I have encountered many, and everytime I never get perfect answer by myself. Once i get the answer, everything seems very logic, it's just so hard to get there. So Pam, im just wondering if you could post any good question regarding to gene cloning (functional, positional) with the answer=)
Thanks!
sorry...I don't recall that there was a practice midterm posted on the biol 335 website before. does anyone know if it is still there...cause I can't seem to find the link to it..
thanks
Hey Pam,
Just wondering for Q6b regarding the development questions by Dr.H., shouldn't the answer be that Hb will always be an activator? rather than a inhibitor.
Hi Pam. I am a little confused on what we are suppose to know about Su(var) genes. Are we suppose to know the techniques on how the identified them or just know what Su(var) genes do in general?
Hi Pam;
For the FCD pedigree-molecular markers question, why doesn't the uncle with the het morph have the disease, since the disease is dominant and ppl with the disease in the family should have the same morph right?
what did i do wrong?
For Dr Haughn's questions:
hb can act as an inhibitor or as an activator. For example, if it binds to H2, then it will prevent bcd from binding to B1, so it will effectively act as an inhibitor
No need to know about the Su(var)s. Just know that you can use a genetic screen to find genes that codes for proteins with a certain function.
The FCD question:
I assume you are talking about individual 3 in generation II. he does not have the disease, so he must have received his "high band" from his dad (who does not have the disease either) and his "low bands" from his mom, who has the disease allele on the chromosome that has the "high band".
The mom and dad of II-3 (people 1 and 2 in generation I) are actually coming from two distinct families: in the dad's family there is no disease, but people still have the polymorphisms!
I hope this helps
Hi Pam,
I was just doing one of the problems you gave us about swapping the 3' UTRs of bcd and nos and how that would affect the phenotype the embryo of a female homozygous mutant for bcd and nos and carries both swap constructs... I have written down that they would have "no nos and no bcd".. but I'm not sure if this is correct. If it is, why? and If it's not.. what's the correct answer??
Just want to clarify, isn't the FCD on the mother carried on the "low band"? Since the "low band" homozygous sister (II2) has inherited the disease while the "high band" homozygous sister (II1) do not have the disease.
So II3 do not have the disease becase he received his "low band" from dad and "high band" from mom, both of which are not linked to the FCD allele. While II4 received his "high band" from dad and "low band" from mom (which carries the domiant FCD allele).
One thing I am still confused about this question is that, if this disease is dominant, then how come it is still "rare"? Since only one copy of its allele is required for phenotypical expression, meaning that 50% of progeny between a cross of heterozygous (FCD/fcd) parent and homozygous (fcd/fcd) parent will have this disease, which is quite a high ratio.
i think the rare is due to "this is a rare disease" we had that in 334
FCD questions:
the fact that an allele is rare does not mean it can't be dominant! It just means that it's an allele that very, very few people have in the whole population. It is an important piece of information to know when we solve pedigrees, because it allows us to assume that all the people who "marry in" into a family are homozygous for the frequent allele-unless there is direct evidence for the contrary.
Cheers
About the swapped nos and bcd:
(the first question on the sheet that had 2 questions)
--> The embryo does not have bcd or nos OF ITS OWN, or FROM ITS OWN MOM.
The only bcd and nos that it has, are the ones with the swapped 3'UTRs.
That's what your notes meant, I assume.
Cheers-and get some rest now!
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