my parting gift in case it wasnt in the answers....
tata pple!!
a blog site for this trip.
http://www.travelpod.com/members/chansensei
I think I am so going to be dead!
I think I am so going to be dead!
Odd Stuff
One is a limpet and the other barnacle. Which is which?
From Evol 2 again
Qn23: clarification. It is onto not ortho-logy.
Ontology is developmental biology:
The theory of recapitulation, also called the biogenetic law or embryological parallelism, and often expressed as "ontogeny recapitulates phylogeny.
But is of course refuted on many fronts (so is not important)
The recapitulation theory claims that each successive stage in the development of an individual represents one of the adult forms that appeared in its evolutionary history.
(This idea is too extreme! If this is true, we will have real gills which close up later during embryo devt!)
Modern observation
Species which have an evolutionary relationship typically share the early stages of embryonal development and differ in later stages. Examples include:
• The backbone, the common structure among all vertebrates such as fish, reptiles and mammals, appears as one of the earliest structures laid out in all vertebrate embryos.
If a structure vanished in an evolutionary sequence, then one can often observe a corresponding structure appearing at one stage during embryonic development, only to disappear or become modified in a later stage. Examples include:
• Whales, which have evolved from land mammals, don't have legs, but tiny remnant leg bones lie buried deep in their bodies. During embryonal development, leg extremities first occur, then recede. Similarly, whale embryos have hair at one stage (like all mammalian embryos), but lose most of it later.
• The common ancestor of humans and monkeys had a tail, and human embryos also have a tail at one point; it later recedes to form the coccyx.
In other words: there is embryological devt does not show us the actual evol history.
Qn7: The simplest organism is found at the end of a tree. Which end?(hint: How does a real tree look like?) – towards the pointed end of a V-shape
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Jane was asking about some questions on the cloning and gene therapy MCQs. I will post it up once i have time. Seemed like I have to do it while overseas cos i am really rushed for time here :P
H3 bio also......
Let me pack first k? I havent even settle lodging yet so.....shucks!!!!!
A few good question from 3B and random voices from the grapevines
1) (molecular clock) How can we reconcile the generation time and mutation rate of a particular gene. If a common gene is found in bacteria and an eukaryote, given the relative fast reproduction rate of bacteria, shouldn't the gene accumulate more mutations over the same time span and if so, how does that allow us to decide the point of divergence?
Ans: the generation time and rate of mutation is normalised for a valid comparison to be made btw different organisms!! =)
2) (not impt) why is there two origin of replication in pBluescript?
Ans: Pls ignore f1 origin. pBluescript is what we called a phagemid: a hybrid betw phage and plasmid.
- WIKI: http://en.wikipedia.org/wiki/Phagemid
A phagemid or phasmid is a type of cloning vector developed as a hybrid of the filamentous phage M13 and plasmids to produce a vector that can grow as a plasmid, and also be packaged as single stranded DNA in viral particles. Phagemids contain an origin of replication (ori) for double stranded replication, as well as an f1 ori to enable single stranded replication and packaging into phage particles
3) Co-evolution
Each party in a coevolutionary relationship exerts selective pressures on the other, thereby affecting each others' evolution. e.g parasite or mutualism relationship
4) why is the size of the cloning vector important? (sensei)
together with the gene of interest, it is advisable not to have the recombinant plasmid at too biga size because small means higher copy number, greater stability and greater transformation efficiency.
5) why is it that HIV RT is a 3-in-1 model while the RT in cloning we still need to remove RNA (from RNA:DNA hybrid) with RNase H and later use DNA polymerase?
The RT in cloning is a different version and we choose not to use it because if the enzyme has multiple functions, its efficiency (less cDNA) can be compromised when it choose to degrade the RNA of the PolyA tail:OligerT DNA primer instead of elongating the DNA chain.
6) Using terminal transferase: how is the length of CCC or GGGGG ensured (if it is)
ANS: It isn't. They may not be heavenly made matches in terms of length but the gaps at the ends of the 5' strands can be filled in with nucleotides under the catalytic action of DNA polymerase and the nicks in the strands were sealed by DNA ligase.
Ans: the generation time and rate of mutation is normalised for a valid comparison to be made btw different organisms!! =)
2) (not impt) why is there two origin of replication in pBluescript?
Ans: Pls ignore f1 origin. pBluescript is what we called a phagemid: a hybrid betw phage and plasmid.
- WIKI: http://en.wikipedia.org/wiki/Phagemid
A phagemid or phasmid is a type of cloning vector developed as a hybrid of the filamentous phage M13 and plasmids to produce a vector that can grow as a plasmid, and also be packaged as single stranded DNA in viral particles. Phagemids contain an origin of replication (ori) for double stranded replication, as well as an f1 ori to enable single stranded replication and packaging into phage particles
3) Co-evolution
Each party in a coevolutionary relationship exerts selective pressures on the other, thereby affecting each others' evolution. e.g parasite or mutualism relationship
4) why is the size of the cloning vector important? (sensei)
together with the gene of interest, it is advisable not to have the recombinant plasmid at too biga size because small means higher copy number, greater stability and greater transformation efficiency.
5) why is it that HIV RT is a 3-in-1 model while the RT in cloning we still need to remove RNA (from RNA:DNA hybrid) with RNase H and later use DNA polymerase?
The RT in cloning is a different version and we choose not to use it because if the enzyme has multiple functions, its efficiency (less cDNA) can be compromised when it choose to degrade the RNA of the PolyA tail:OligerT DNA primer instead of elongating the DNA chain.
6) Using terminal transferase: how is the length of CCC or GGGGG ensured (if it is)
ANS: It isn't. They may not be heavenly made matches in terms of length but the gaps at the ends of the 5' strands can be filled in with nucleotides under the catalytic action of DNA polymerase and the nicks in the strands were sealed by DNA ligase.
Comments for the week
A few things to run through for the week on mock and evol:
Mock:
(esp to Jane)
Absorbency is not the equivalent of wavelength. It is more related to intensity.
But let's us examine what is intensity first -a greater intensity of light means having more photons (increased conc) to strike a surface.
Compare this with wavelength - the wavelength of light will determine the amount of energy the photons will carry.
Therefore, having a higher intensity of light at a particular wavelength means having more photons of a particular energy.
How is this related to absorbancy?
The maximum absorbance of a plant is determined by the photosynthetic pigments it contains. If you shine blue light at it, how much of the energy can it absorb? If you start at low intensity, the plant can probably photosynthesize more if you increase intensity until other limiting factor comes into play.
you may ask: but didnt we fix the intensity of the light?
Yup you did but a plant will have difficult capacity to absorb different colored light (diff wavelength). For green color , you may need x photons to reach max, but for blue you may need 10x photons to hit its max so while the intensity of the light has been fixed, the effect on the rate of photosynthesis due to diff colored light will differ and each of them has it own max absorbance before other limiting factor comes to play. So if intensity is not high enough, you may give same rate of photosynthesis for different colored light because one may have reached its max while the other has not.
-----------------
Evol
The story of marsupial. It was once thought (and perhaps still so) that marsupials are the ancestors of placental mammals but evidence is emerging to suggest that these two groups branch off at about the same time.
But they are still deliberating on why Marsupial are found in high conc in Australia: the drift? different selection pressure? or both?
http://www.ucmp.berkeley.edu/mammal/marsupial/marsupial.html
http://en.wikipedia.org/wiki/Marsupial
http://bcb705.blogspot.com/2006/05/continental-drift-marsupials-and.html
---------------
a few highlights we have learnt from Evol - just to clarify:
1) there is something called the species-area relationship: in short, when you looked a group of islands, you have to consider the size of it and the distance it is from the main island to predict variety of species
2) For neutral mutations, the key is really having no effect on fitness
For a mutation that leads to no change in phenotype, it is definitely neutral since there would not be a change in fitness either.
But mutations that do affect phenotype in measurable ways but do not affect the organism's fitness should also be considered as neutral.
It is definitely reasonable to do so because that will account for variants we see in our population due to spontaneous mutation. But we will consider it as a minor for now.
We often work with "no change in phenotype' as in the notes because that was what Kimura first proposed and most probable since it is considerably rare to have a change in phenotype without affecting fitness - although not impossible.
---------
Reiterate:
Evo MCQs Part 2.
32: (A) - bcos the question compared "btw" population. each population will see an increased in genetic variation but btw population, there is less distinction since they each now shared certain common alleles/genes.
--------
A question came to mind by alicia some time back:
How does membrane-bound AChE hydrolyse ACh? How can persistent signaling be achieved?
If they are membrane-bound, how do they hydrolyse ACh? If all ligand-receptor interaction is transient, how can there be persistent signaling?
The binding of ligand and receptor is indeed transient. What AChE offer to do is to hydrolyse free ACh so that the concentration of ACh in synaptic cleft increases for an increased probability of binding of the ligand to receptor and thus an observed substained signaling (the reversible reaction is less likely to go backward yah?) Persistence in signal does not refer to a tighter binding but increased probability/prolonged of so.
Mock:
(esp to Jane)
Absorbency is not the equivalent of wavelength. It is more related to intensity.
But let's us examine what is intensity first -a greater intensity of light means having more photons (increased conc) to strike a surface.
Compare this with wavelength - the wavelength of light will determine the amount of energy the photons will carry.
Therefore, having a higher intensity of light at a particular wavelength means having more photons of a particular energy.
How is this related to absorbancy?
The maximum absorbance of a plant is determined by the photosynthetic pigments it contains. If you shine blue light at it, how much of the energy can it absorb? If you start at low intensity, the plant can probably photosynthesize more if you increase intensity until other limiting factor comes into play.
you may ask: but didnt we fix the intensity of the light?
Yup you did but a plant will have difficult capacity to absorb different colored light (diff wavelength). For green color , you may need x photons to reach max, but for blue you may need 10x photons to hit its max so while the intensity of the light has been fixed, the effect on the rate of photosynthesis due to diff colored light will differ and each of them has it own max absorbance before other limiting factor comes to play. So if intensity is not high enough, you may give same rate of photosynthesis for different colored light because one may have reached its max while the other has not.
-----------------
Evol
The story of marsupial. It was once thought (and perhaps still so) that marsupials are the ancestors of placental mammals but evidence is emerging to suggest that these two groups branch off at about the same time.
But they are still deliberating on why Marsupial are found in high conc in Australia: the drift? different selection pressure? or both?
http://www.ucmp.berkeley.edu/mammal/marsupial/marsupial.html
http://en.wikipedia.org/wiki/Marsupial
http://bcb705.blogspot.com/2006/05/continental-drift-marsupials-and.html
---------------
a few highlights we have learnt from Evol - just to clarify:
1) there is something called the species-area relationship: in short, when you looked a group of islands, you have to consider the size of it and the distance it is from the main island to predict variety of species
2) For neutral mutations, the key is really having no effect on fitness
For a mutation that leads to no change in phenotype, it is definitely neutral since there would not be a change in fitness either.
But mutations that do affect phenotype in measurable ways but do not affect the organism's fitness should also be considered as neutral.
It is definitely reasonable to do so because that will account for variants we see in our population due to spontaneous mutation. But we will consider it as a minor for now.
We often work with "no change in phenotype' as in the notes because that was what Kimura first proposed and most probable since it is considerably rare to have a change in phenotype without affecting fitness - although not impossible.
---------
Reiterate:
Evo MCQs Part 2.
32: (A) - bcos the question compared "btw" population. each population will see an increased in genetic variation but btw population, there is less distinction since they each now shared certain common alleles/genes.
--------
A question came to mind by alicia some time back:
How does membrane-bound AChE hydrolyse ACh? How can persistent signaling be achieved?
If they are membrane-bound, how do they hydrolyse ACh? If all ligand-receptor interaction is transient, how can there be persistent signaling?
The binding of ligand and receptor is indeed transient. What AChE offer to do is to hydrolyse free ACh so that the concentration of ACh in synaptic cleft increases for an increased probability of binding of the ligand to receptor and thus an observed substained signaling (the reversible reaction is less likely to go backward yah?) Persistence in signal does not refer to a tighter binding but increased probability/prolonged of so.
Such a Crappy Week
i think it all started with the loss of the game. The weight of it all loads up on the chest and it was a difficult period (together with other stuff) and I still feel it even though I am slowly dissolving it into another learning point, another thing to ponder over. maybe retail therapy tmr will help.
it is not about the winning or the losing. It was the lack of spirit from the players and my own haplessness. As I sit in the chair under the sun, squinting to watch the games, there are moments when I thought: should I stand up and shout at them,should I rally them up for an inspirational moment? M I just going to sit here and do nothing. In the end that is all i did - sit there but i figured I am really not an inspiring person because I am not really articulate enough. And I really can't scold them because I don't know how to even though I am mad at them for not living it up to themselves and their abilities. The scolding? I left that to coach.
I was seething because I wanted these kids to win, to bring it home for themselves and not for me. 6 years of games and I hoped this year will be the year that they can finally find themselves in a final to play the greatest game in their 6 years. There is such a good chance this year after working on getting in the DSA, the arrangement for Sat trainings and all the favours I pulled . But they blew it - at least for now - because they din have the heart to make it work.
I felt a little betrayed but more than ever, sad - for them for the defeat that should not have been. I asked: can I do better? what should I have done? Did I miss something out? Maybe I did. Maybe I didn't.
A student told me I was hard on myself. And it is difficult not to maybe because I recalled the difficulties I once had and dont want others to experience that misery I had.
Then come the lessons. you just know it when you are out of sorts. It has been a while since I felt that but it came back and the lessons were horrible I thought. I don' think anyone was listening or convinced for neither am I. So I looked at my classes and go with the theme of the week: can I do better? what is going wrong? is it inexperience and the lack of sound methodology? too emo?
Then I saw my colleagues coming up with this and that for their classes and suddenly I felt that I shouldnt be taking my classes because they deserve better.
Towards the end of this entry, I suddenly recall what I have been reading (again) recently: that the most important person to give your compassion to is to yourself. Because too very often, we are too harsh on ourselves.
So let's take a break. treat ourselves a little/more better.
it is not about the winning or the losing. It was the lack of spirit from the players and my own haplessness. As I sit in the chair under the sun, squinting to watch the games, there are moments when I thought: should I stand up and shout at them,should I rally them up for an inspirational moment? M I just going to sit here and do nothing. In the end that is all i did - sit there but i figured I am really not an inspiring person because I am not really articulate enough. And I really can't scold them because I don't know how to even though I am mad at them for not living it up to themselves and their abilities. The scolding? I left that to coach.
I was seething because I wanted these kids to win, to bring it home for themselves and not for me. 6 years of games and I hoped this year will be the year that they can finally find themselves in a final to play the greatest game in their 6 years. There is such a good chance this year after working on getting in the DSA, the arrangement for Sat trainings and all the favours I pulled . But they blew it - at least for now - because they din have the heart to make it work.
I felt a little betrayed but more than ever, sad - for them for the defeat that should not have been. I asked: can I do better? what should I have done? Did I miss something out? Maybe I did. Maybe I didn't.
A student told me I was hard on myself. And it is difficult not to maybe because I recalled the difficulties I once had and dont want others to experience that misery I had.
Then come the lessons. you just know it when you are out of sorts. It has been a while since I felt that but it came back and the lessons were horrible I thought. I don' think anyone was listening or convinced for neither am I. So I looked at my classes and go with the theme of the week: can I do better? what is going wrong? is it inexperience and the lack of sound methodology? too emo?
Then I saw my colleagues coming up with this and that for their classes and suddenly I felt that I shouldnt be taking my classes because they deserve better.
Towards the end of this entry, I suddenly recall what I have been reading (again) recently: that the most important person to give your compassion to is to yourself. Because too very often, we are too harsh on ourselves.
So let's take a break. treat ourselves a little/more better.
Questions on Cloning notes
Someone asked:
we have used lac and trp operon in synthesizing human growth factor/ insulin and anti-thrombin. Does it matter which operon is used?
Ans: Nope. Don't worry about it because the examples are given because that was just what people had worked with in making those protein. By now, I am sure things have moved on and they may be using other operons. =)
Can we use a RNA primer?
Does it matter if we have a RNA:DNA hybrid if we just want to check the sequence?
Ans:It doesnt really matter just that there is no reason to have such a hybrid. Why use RNA when DNA primers can also be readily synthesized?
Also, will we have end-replication problem if we use RNA primers?
Ans: No, because there will not be any DNA polymerase coming along behind the primer to remove it and fill the space with DNA. so The primers will flank the sequence/gene of interest.
we have used lac and trp operon in synthesizing human growth factor/ insulin and anti-thrombin. Does it matter which operon is used?
Ans: Nope. Don't worry about it because the examples are given because that was just what people had worked with in making those protein. By now, I am sure things have moved on and they may be using other operons. =)
Can we use a RNA primer?
Does it matter if we have a RNA:DNA hybrid if we just want to check the sequence?
Ans:It doesnt really matter just that there is no reason to have such a hybrid. Why use RNA when DNA primers can also be readily synthesized?
Also, will we have end-replication problem if we use RNA primers?
Ans: No, because there will not be any DNA polymerase coming along behind the primer to remove it and fill the space with DNA. so The primers will flank the sequence/gene of interest.
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