So I was right even tho my frame of mind is not.
From notes:
1) It is not telomeric DNA per se, but rather the association of an ensemble of proteins with telomeric DNA, that is essential for the formation of a protective cap structure. In human cells, a central component of the end-capping structure is the telomeric double-stranded DNA binding protein TRF2.
TRF2 is actually an important protein for this capping structure alto we did not talk much about it
2) Does Satelite DNA have high incidence of AT sequences?
There must be something unique about satelite DNA to make it stand out (a separate band from the rest of the genome).
Satelite DNA can have AT-rich sequences or GC-rich sequences, depending on the basic unit of a tandem repeat.
they just dun get it
Sometimes or many times, we dun get what we want.
I know because I used to fight for my rights and my vindication, and defeats came crashing by.
I remembered it as a difficult taste to swallow each time when you tried and tried yet there are things that you cannot overcome.
But in retrospect, it is all part of growing up. it reminded us not to give up and keep on trying becos there is always hope for the opportunity. I guess that will be the lesson I want my kids to learn when i refused to buckle and give them the extra credits even tho i sympathised, to be fair to others . they are probably cursing and swearing behind my back because i dun think they see the way i do
so me too, am learning that some lessons are just harder to deliver for I felt the strain on the relationship.
I think I am just trying too hard sometimes. trying to deliver opportunities to them, offering them choices, for things that I never get to do in my time Perhaps I will just let it be. For it will be easier.
I know because I used to fight for my rights and my vindication, and defeats came crashing by.
I remembered it as a difficult taste to swallow each time when you tried and tried yet there are things that you cannot overcome.
But in retrospect, it is all part of growing up. it reminded us not to give up and keep on trying becos there is always hope for the opportunity. I guess that will be the lesson I want my kids to learn when i refused to buckle and give them the extra credits even tho i sympathised, to be fair to others . they are probably cursing and swearing behind my back because i dun think they see the way i do
so me too, am learning that some lessons are just harder to deliver for I felt the strain on the relationship.
I think I am just trying too hard sometimes. trying to deliver opportunities to them, offering them choices, for things that I never get to do in my time Perhaps I will just let it be. For it will be easier.
hospice
Visited my fren's mum this afternoon after hearing news that she has taken a turn for the worse last night.
battling colon cancer for 3 years, she has almost reached the end of the road as my fren and his sister stay vigilant by her side.
But what caught me off-guard was how different auntie looked.
she looked nothing like the lady I once knew when I visited my fren in the past (since sec sch)
She now looks like any other patients, bedridden, sunken and shriveled - a lost page in my memory.
Bringing tea for my friend and her sister, I eventually bade farewell to auntie,
Lost to the world in that morphine-induced bliss.
battling colon cancer for 3 years, she has almost reached the end of the road as my fren and his sister stay vigilant by her side.
But what caught me off-guard was how different auntie looked.
she looked nothing like the lady I once knew when I visited my fren in the past (since sec sch)
She now looks like any other patients, bedridden, sunken and shriveled - a lost page in my memory.
Bringing tea for my friend and her sister, I eventually bade farewell to auntie,
Lost to the world in that morphine-induced bliss.
AFter tutorial clarifications
Just to recap and consolidate:
Hayflick limit : cell division limit =
critical length of the telomeres we have been talking about.
This is in response to GY's question: when you reach the critical length of telomeres and enter a state of cell senescence, do you also undergo apoptosis? (good one!)
When telomeres of cells reach Hayflick limit/critical lengths, it enters cellular/replicative senescence (an inability to divide) or apoptosis.
Senescence and Apoptosis are different situations and either case will take place depending on cellular conditions.
Hayflick limit : cell division limit =
critical length of the telomeres we have been talking about.
This is in response to GY's question: when you reach the critical length of telomeres and enter a state of cell senescence, do you also undergo apoptosis? (good one!)
When telomeres of cells reach Hayflick limit/critical lengths, it enters cellular/replicative senescence (an inability to divide) or apoptosis.
Senescence and Apoptosis are different situations and either case will take place depending on cellular conditions.
Questions of the Week
Contributed by ST:
> 1) are enhancers and silencers found within or between genes?
Both are be found anywhere- in non-coding regions (betw genes) or within genes (in the introns) But we recognise that enhancers are distal elements (pretty far away from the promoter). Little is said about silencers so we gather that they do not have to be distal.
> 2) when saying that the transposable elements are repetitive DNA, does it mean that they are a long string of repeated nucleotides, e.g. CAGCAGCAGCAG or is it because there are multiple copies of transposons scattered throughout the genome (due to the copy and paste mechanism of retrotransposons) ?
Thanks for clarifying this! I noticed this while checking the notes and wanted to point this out!
Transposons does not have tandem repeat. Its basic characteristic is in its ability to jump! The notes could be clearer: the "repetitive" part is really about the many copies that can exist due to the copy and paste mechanisms of retrotransposons which so very common in us. So you are right!
> 3) "Telomeres do not exist as a free end, but as a loop - formed when the 3' single-stranded ends DISPLACES the same sequence in an upstream region of the telomere, causing a single-stranded region to form." I don't really get the bolded parts.
The 3'OH overhang will displace an identical sequences upstream (of ssDNA 1) to form complementary base-pairing with the other DNA strand (ssDNA2). The displaced single-stranded DNA (ssDNA) which of the same sequences as the 3'OH overhang is now left hanging like a hump-like structure you see in your notes because it has no one to base-pair with.
> 4) what is the relationship/difference between gene amplification and gene duplication?
gene amplification usually imply multiple copies (more than 2).
gene duplication is only 2 copies.
But that being said, this is however not necessarily true in the case of cancer study where gene duplication is already considered as gene amplification since an extra copy of the gene is usually sufficient to wreak havoc in your cells.
So check the context although it is usually not an issue
> 5) How does the development of tumours support natural selection? Why do cancer cells have better growth advantage?
the growth advantage comes with mutations (that can benefit of cos!).
With accumulated mutations (that can only exist because the cells do not die readily as seen in tumor cells), some of these cells have been altered such that they are better at surviving e.g. use less resources to survive and are able to outcompete others and dominate.
This is natural selection at the molecular scale!
> 1) are enhancers and silencers found within or between genes?
Both are be found anywhere- in non-coding regions (betw genes) or within genes (in the introns) But we recognise that enhancers are distal elements (pretty far away from the promoter). Little is said about silencers so we gather that they do not have to be distal.
> 2) when saying that the transposable elements are repetitive DNA, does it mean that they are a long string of repeated nucleotides, e.g. CAGCAGCAGCAG or is it because there are multiple copies of transposons scattered throughout the genome (due to the copy and paste mechanism of retrotransposons) ?
Thanks for clarifying this! I noticed this while checking the notes and wanted to point this out!
Transposons does not have tandem repeat. Its basic characteristic is in its ability to jump! The notes could be clearer: the "repetitive" part is really about the many copies that can exist due to the copy and paste mechanisms of retrotransposons which so very common in us. So you are right!
> 3) "Telomeres do not exist as a free end, but as a loop - formed when the 3' single-stranded ends DISPLACES the same sequence in an upstream region of the telomere, causing a single-stranded region to form." I don't really get the bolded parts.
The 3'OH overhang will displace an identical sequences upstream (of ssDNA 1) to form complementary base-pairing with the other DNA strand (ssDNA2). The displaced single-stranded DNA (ssDNA) which of the same sequences as the 3'OH overhang is now left hanging like a hump-like structure you see in your notes because it has no one to base-pair with.
> 4) what is the relationship/difference between gene amplification and gene duplication?
gene amplification usually imply multiple copies (more than 2).
gene duplication is only 2 copies.
But that being said, this is however not necessarily true in the case of cancer study where gene duplication is already considered as gene amplification since an extra copy of the gene is usually sufficient to wreak havoc in your cells.
So check the context although it is usually not an issue
> 5) How does the development of tumours support natural selection? Why do cancer cells have better growth advantage?
the growth advantage comes with mutations (that can benefit of cos!).
With accumulated mutations (that can only exist because the cells do not die readily as seen in tumor cells), some of these cells have been altered such that they are better at surviving e.g. use less resources to survive and are able to outcompete others and dominate.
This is natural selection at the molecular scale!
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