You inverted lagging/leading strands. The leading strand is the one being synthesized continuously (even its RNA primer is replaced by dNTPs). The lagging strand however is synthesized with multiple primers in the form of Okazaki fragments, the final primer being removed on the 5' end, making the lagging strand shorter.
Hi there, leading-strand synthesis generates a blunt end while lagging-strand synthesis produces a long G-rich 3′ overhang, and suggest that variations in lagging-strand synthesis may regulate the rate of telomere shortening in normal diploid human cells. The article supporting this statement is www.ncbi.nlm.nih.gov/pmc/articles/PMC316649/ If you can specify the mistake you detected, we will gladly take a look at that and amend the problem. Thank you
@@EasyPeasyLearning Could you explain why? I’m a graduate student in mol bio and I have always been taught that the lagging strand is shorter. Which makes complete sense since its 5’ primer is removed at the end of synthesis. My question to you is why do you think the lagging strand and not the leading strand makes a 3’ overhang?
Hi Raphael, you are mixing 2 different concepts. The 1st concept is that the 3' overhang is on the lagging-strand and the second concept is that after replication the telomere overhang lose a part of DNA due to okazaki fragments. Think it this way if the shorter strand start losing its part of DNA then the quality of life will remain for short time only. Telomere overhang have sequence that is not translating the essential proteins, so losing them little bit is not affecting our quality of life until it reaches the crucial part where it stops dividing anymore. Hope that will clear the confusion.
@@EasyPeasyLearning I discussed with my professor who confirmed my points. Many other people also pointed this in the comments. The leading strand is longer. Its overhang is then extended by telomerase to leave more room for polymerase to synthesize the complementary strand
I'm so grateful for your video. I'm struggling with telomere and telomerase until I watch this video. But there is a little mistake in your video - the RNA template, I think it would be Uracil, not Thymine. However, thank you soooooo muchhh
I think some of your concepts are confused. Please refer to a genetics textbook. The leading strand is 3' to 5' and it is synthesized in the 5' to 3' direction. The 5' end of each DNA strand has a primer removed and that leaves the overhang, which is corrected by telomerase, which repairs the overhang.
This is a good explanation. But the lagging strand should be the one that was actually lagging (Okazaki fragments) which is the black one not the red one. Hope you fix that.
Thank you! but I don’t understand.. what about the 5’ tip of the leading strand that appears after removing the primer?! How would the DNA polymerase add to 5’ of the leading strand? Does the same thing of Telomerase happen in this part?
hello i know you asked this question 9 months ago but to answer it, after the primer gets removed, a DNA polymerase with 5’ to 3’ exonuclease activity will replace the primer with DNA versions
it was perfect. one question is about that kind of people who lives longer than others for example they are more than 100 years old, Does not their telomeres shorten?
Hi Paniz! The time span of telomere shortening varies from person to person. It can depend on different factors like atmosphere, food, weather, physical activity etc etc.
Hi Eda, think it of this way. New strand always get synthesize from 5' to 3' end. Then which strand can make it without problem ? that is 3' to 5' so it is a leading strand. Furthermore look at the textbook again the confusion will get clear. Here i am giving a reference from 1 site. www.quora.com/Why-does-the-lagging-strand-of-DNA-have-to-be-discontinuous Still the confusion remains there. You can contact me again.
@@EasyPeasyLearning Yes, new strand always synthesize from 5’ to 3’ . My point is the new 3’-5’ strand that synthesized from 5’-3’ parental strand will synthesize as okazaki fragments so we need a new short RNA for every new Okazaki fragment. When it is time to synthesize tip of new 3’-5’ strand the RNA Primase couldn’t synthesize the tip so we lose telomeric G-tail from parental 5’-3’ strand in every division. We use telomerase to prevent that. So the problem should be in the new and 3’-5’ strand.
Hi Eda, here it needs to be corrected. New okazaki fragments appear on lagging strand is not from 3' to 5'. It is also from 5' to 3' on the parental strand that is also from 5' to 3'. That is why they are in pieces and need primer again and again. This is the detailed article on replication www2.csudh.edu/nsturm/CHEMXL153/DNASynthesis.htm
are there techniques to shorten telomeres? with proteins? when the DNA is in the histons, are the telomeres outside it? at the end? and can they be attacked then?
Hi Psychologie The advent of the clustered regularly interspaced short palindromic repeats/CRISPR-associated (CRISPR/Cas) system has led to a wide array of targeted genetic studies that are already being employed to modify telomeres and telomerase, as well as the genes that affect them. The article supporting this statement is www.ncbi.nlm.nih.gov/pmc/articles/PMC6406488/ Telomeres normally would not get attacked by nucleases present inside our cell due to the knot made by telomere in the end. Lastly the query about histone attachment with telomere, Specific post-translational modifications of histones, including methylation, acetylation, and ubiquitination, have been shown to be necessary for maintaining a chromatin environment that promotes telomere integrity. The article supporting this statement is www.ncbi.nlm.nih.gov/pmc/articles/PMC6407025/
Hi Psychologie Why don't you ask your questions on our community page. Every subscriber can participate in that and it will be a healthy activity for everyone.
Hey I got one question you said that in telomerase is RNA plus protein so there is uracil instead of thymine but in the video it’s not is it wrong or…?
Hi there, this article might help you in understanding the concept better www.ncbi.nlm.nih.gov/pmc/articles/PMC7152597/#:~:text=Non%2Dcoding%20RNAs%20critically%20regulate,to%20cellular%20senescence%20and%20aging.
The labeling of the lagging/leading strand is inverted. The leading strand is linearly synthesized by DNA polymerase 5'->3'. Telomerase recognizes the overhang of the leading strand and extends it to repair telomere length, after which RNA primase can add RNA primers to assist DNA polymerase in synthesizing the lagging strand. For structural reasons, both in the case of normal DNA replication and extension of the telomere, RNA primase cannot build the RNA primer at the end of the DNA making the lagging strand shorter. That is part of the reason why the lagging strand is shorter than the leading strand, the other is that nucleases actively shorten then lagging strand to form the t loop structure.
Hi there, leading-strand synthesis generates a blunt end while lagging-strand synthesis produces a long G-rich 3′ overhang, and suggest that variations in lagging-strand synthesis may regulate the rate of telomere shortening in normal diploid human cells. The article supporting this statement is www.ncbi.nlm.nih.gov/pmc/articles/PMC316649/ If you can provide the article claiming that leading strand have overhang, we will gladly want to look upon it and if your statement is true, we will surely amend the video. Thank you
@@EasyPeasyLearning These are two very concepts. Telomere elongation happens just after DNA replication, so strictly speaking the leading and lagging strands do not appear as shown in the video. the newly synthesized leading strand is in complex with its parental strand, and this duplex consists of equal length strands prior to the involvement of telomorase. The newly synthesized lagging strand is similarly in complex with its parental strand, but here the parental strand is longer than the newly synthesized strand (i.e. there is overhang). Instead of labeling the strands in these duplexes as lagging and leading strands, it's better to follow literature convention and name them either 3' and 5' strand or G-strand and C-strand. Alternatively, the strands in the video could be labeled parental strand and newly synthesized lagging strand, as that is the pairing shown. The parental strand is then of course the longer G-rich strand strand ending in 3'. So the concept that the lagging strand has a longer overhang compared to the leading strand is true, but that refers to the duplex of the lagging strand and its template compared to the leading strand and its template. It does not refer to the overhang between two strands in duplex as presented in the video. This confusion likely resulted from mislabeling these strands as leading and lagging, as discussed before. See this image for a schematic view: www.cell.com/fulltext/S0092-8674(09)00897-6
Thank you very much for providing the information. We will definitely look into it and correct everything accordingly. We appreciate your support and feedback.
Lagging strand is longer to make a knot at the end of a chromosome so that the Dnase enzymes can't degrade it if its open. It is also longer then the leading strand so the telomere depletion would not affect the real Gene's present on the chromosome for a certain period of time.
Hi Tony, This article will help you understand it. www.nature.com/scitable/topicpage/telomeres-of-human-chromosomes-21041/ www.intechopen.com/chapters/41797
@@EasyPeasyLearning Your source says the leading strand is longer "Thus, as the replication fork moves along the chromosome, one of the two daughter strands is synthesized continuously. The other daughter strand, known as the lagging strand, is synthesized discontinuously in short fragments known as Okazaki fragments, each of which has its own RNA primer. The RNA primers are subsequently degraded, and the gaps between the Okazaki fragments are then filled in by the DNA repair machinery. A problem arises at the end of the chromosome, however, because the DNA repair machinery is unable to repair the gap left by the terminal RNA primer. Consequently, the new DNA molecule is shorter than the parent DNA molecule by at least the length of one RNA primer. Without a solution to this end-replication problem, chromosomes would progressively shorten over many cell divisions, a process that would bring about catastrophic consequences."
I was trying to understand the concept of telomeres from such a long time and this video made it crystal clear! Thank you so much!
You are welcome 😊
Thank you so much to clear my doubts regarding replication termination
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Now that was perfect . Hope to see these types of explanations for more topics
Thank you 😊
It's believed that because of the shortening of Telomere, the generations now look shorter than before. Thank you for the great videos
This is the best video that has answered all inquiries I have been having. Thank you so much.
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Thank you so much...This was a core concept .but you explained it beautifully ...
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omg thank you so much i just started my masters degree and i couldn’t find videos with enough details about this
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Thank you !!! You actually made this topic easy peasy💛💛
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Thank you so much for simplifying this topic i now understand it
Thank you 😊
I really like this video, thank you so much. I understand clearly now.
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Wow! What amazing presentation. Thank you so much.
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You inverted lagging/leading strands. The leading strand is the one being synthesized continuously (even its RNA primer is replaced by dNTPs). The lagging strand however is synthesized with multiple primers in the form of Okazaki fragments, the final primer being removed on the 5' end, making the lagging strand shorter.
Hi there,
leading-strand synthesis generates a blunt end while lagging-strand synthesis produces a long G-rich 3′ overhang, and suggest that variations in lagging-strand synthesis may regulate the rate of telomere shortening in normal diploid human cells.
The article supporting this statement is
www.ncbi.nlm.nih.gov/pmc/articles/PMC316649/
If you can specify the mistake you detected, we will gladly take a look at that and amend the problem.
Thank you
@@EasyPeasyLearning Could you explain why? I’m a graduate student in mol bio and I have always been taught that the lagging strand is shorter. Which makes complete sense since its 5’ primer is removed at the end of synthesis. My question to you is why do you think the lagging strand and not the leading strand makes a 3’ overhang?
Hi Raphael, you are mixing 2 different concepts. The 1st concept is that the 3' overhang is on the lagging-strand and the second concept is that after replication the telomere overhang lose a part of DNA due to okazaki fragments.
Think it this way if the shorter strand start losing its part of DNA then the quality of life will remain for short time only. Telomere overhang have sequence that is not translating the essential proteins, so losing them little bit is not affecting our quality of life until it reaches the crucial part where it stops dividing anymore.
Hope that will clear the confusion.
@@EasyPeasyLearning I discussed with my professor who confirmed my points. Many other people also pointed this in the comments. The leading strand is longer. Its overhang is then extended by telomerase to leave more room for polymerase to synthesize the complementary strand
Hi Raphael
If you can provide a scientist article or review paper supporting your statement, we will gladly look into it.
Great video. Nice and neat explanation.
Thank you 😊
Absolutely excellent!
Thank you John 😊
Thak you so much it was so helpful❤
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Thank you very much for explaining
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I'm so grateful for your video. I'm struggling with telomere and telomerase until I watch this video. But there is a little mistake in your video - the RNA template, I think it would be Uracil, not Thymine. However, thank you soooooo muchhh
You are welcome 😊 and thanks for the correction 😊 ☺
Precise video, thank you!!❤
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Omg me encantó el video ❤❤❤❤ Thank youuuuu
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love this explanation!
Thank you 😊
this video was awesome!!! thank you so much!
Thank you
Great explanation !! Thank you !!
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THANK YOU!! you made easy peasy
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Thanks so much, very well explained
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Great explanation ❤
Thank you 😊
Excellent teaching, thanks for this content!
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Excellent! Thanks 🙏
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Thank you so much 😊😊
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this was so helpful, thank you :)
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Very useful!
Thank you 😊
wonderful presentation indeed . congratulations
Thank you
Welcome and continue to share your presentations
You have very clear concepts
I think some of your concepts are confused. Please refer to a genetics textbook.
The leading strand is 3' to 5' and it is synthesized in the 5' to 3' direction.
The 5' end of each DNA strand has a primer removed and that leaves the overhang, which is corrected by telomerase, which repairs the overhang.
I think you mean 3’ not 5’ , right¿
This is a good explanation. But the lagging strand should be the one that was actually lagging (Okazaki fragments) which is the black one not the red one. Hope you fix that.
Thank you for your comment. I will put correction note on it.
Good explain
Thank you 😊
Good media to your take,success for you
great vıdeo, thank you
Glad you liked it!
Amazing!
Thank you 😊
Impressive
Thank you 😊
Thank you! but I don’t understand.. what about the 5’ tip of the leading strand that appears after removing the primer?! How would the DNA polymerase add to 5’ of the leading strand? Does the same thing of Telomerase happen in this part?
hello i know you asked this question 9 months ago but to answer it, after the primer gets removed, a DNA polymerase with 5’ to 3’ exonuclease activity will replace the primer with DNA versions
@@yintiangiam478only dna polymerase 1 do this 5’--3’ exonuclease avtivity
LoL thanks for sharing😊
You are welcome 😊
Thanks a lot
Most welcome
can you please suggest some exercises in molucalar biology !
Please elaborate on how cancer cells and telomere
it was perfect. one question is about that kind of people who lives longer than others for example they are more than 100 years old, Does not their telomeres shorten?
Hi Paniz! The time span of telomere shortening varies from person to person. It can depend on different factors like atmosphere, food, weather, physical activity etc etc.
Thank you but is there something wrong here? I have learned 3’-5’ strand should be lagging and 5’-3’ strand should be leading (parental).
Hi Eda, think it of this way. New strand always get synthesize from 5' to 3' end. Then which strand can make it without problem ? that is 3' to 5' so it is a leading strand. Furthermore look at the textbook again the confusion will get clear. Here i am giving a reference from 1 site.
www.quora.com/Why-does-the-lagging-strand-of-DNA-have-to-be-discontinuous
Still the confusion remains there. You can contact me again.
@@EasyPeasyLearning Yes, new strand always synthesize from 5’ to 3’ . My point is the new 3’-5’ strand that synthesized from 5’-3’ parental strand will synthesize as okazaki fragments so we need a new short RNA for every new Okazaki fragment. When it is time to synthesize tip of new 3’-5’ strand the RNA Primase couldn’t synthesize the tip so we lose telomeric G-tail from parental 5’-3’ strand in every division. We use telomerase to prevent that. So the problem should be in the new and 3’-5’ strand.
Hi Eda, here it needs to be corrected. New okazaki fragments appear on lagging strand is not from 3' to 5'. It is also from 5' to 3' on the parental strand that is also from 5' to 3'. That is why they are in pieces and need primer again and again.
This is the detailed article on replication
www2.csudh.edu/nsturm/CHEMXL153/DNASynthesis.htm
Its not easy peasy unfortunately 😓 thank you for the video tho 😭
I know its really complex but trying my best to make it easy peasy.
Which book do you refer for this topic?
I need video about transposons
Thank you the topic is noted and now is in the queue 😀
Superb
Thank you 😊
Really easy and nice explanation but one doubt not clear as why lagging strand is bigger than leading ...? Not clear
The lagging strand is bigger because it will make up a knot to terminate the process of replication and protect the dna in an intact form (chromosome)
please , do u have video about > Bacterial Transformation: Competence in gram Positive bacteria
thank you
You are welcome 😊
Wow liked it
Thanks
are there techniques to shorten telomeres? with proteins?
when the DNA is in the histons, are the telomeres outside it? at the end? and can they be attacked then?
Hi Psychologie
The advent of the clustered regularly interspaced short palindromic repeats/CRISPR-associated (CRISPR/Cas) system has led to a wide array of targeted genetic studies that are already being employed to modify telomeres and telomerase, as well as the genes that affect them.
The article supporting this statement is
www.ncbi.nlm.nih.gov/pmc/articles/PMC6406488/
Telomeres normally would not get attacked by nucleases present inside our cell due to the knot made by telomere in the end.
Lastly the query about histone attachment with telomere, Specific post-translational modifications of histones, including methylation, acetylation, and ubiquitination, have been shown to be necessary for maintaining a chromatin environment that promotes telomere integrity.
The article supporting this statement is
www.ncbi.nlm.nih.gov/pmc/articles/PMC6407025/
@@EasyPeasyLearning thank you very much! i will look at it. is it also possible to mail you? for asking you some more questions?
@@EasyPeasyLearning hey Easy Peasy, is it possible to ask you something by email?
Hi Psychologie
Why don't you ask your questions on our community page. Every subscriber can participate in that and it will be a healthy activity for everyone.
@@EasyPeasyLearning i understand, but is special question. but is oke
thank u
You are welcome 😊
Hey I got one question you said that in telomerase is RNA plus protein so there is uracil instead of thymine but in the video it’s not is it wrong or…?
Yes, it was a mistake, we did made a correction note on the video but somehow its not visible all the time.
How the terp has thymine istead of uracil when u said its a rna strand pls clarify
It's a mistake in the video, the correction note is already there
shouldn't it be 3'-AAUCCC-5' instead of 3'-AATCCC-5' for the telomerase sequence
Yes you are right it was a mistake in the slide. Thank you for correction
Is aging related to shortining of telomerere or run out of telomeres and become senescent. I mean how could a non-coding DNA prevent aging
Hi there, this article might help you in understanding the concept better
www.ncbi.nlm.nih.gov/pmc/articles/PMC7152597/#:~:text=Non%2Dcoding%20RNAs%20critically%20regulate,to%20cellular%20senescence%20and%20aging.
The labeling of the lagging/leading strand is inverted. The leading strand is linearly synthesized by DNA polymerase 5'->3'. Telomerase recognizes the overhang of the leading strand and extends it to repair telomere length, after which RNA primase can add RNA primers to assist DNA polymerase in synthesizing the lagging strand. For structural reasons, both in the case of normal DNA replication and extension of the telomere, RNA primase cannot build the RNA primer at the end of the DNA making the lagging strand shorter. That is part of the reason why the lagging strand is shorter than the leading strand, the other is that nucleases actively shorten then lagging strand to form the t loop structure.
Hi there,
leading-strand synthesis generates a blunt end while lagging-strand synthesis produces a long G-rich 3′ overhang, and suggest that variations in lagging-strand synthesis may regulate the rate of telomere shortening in normal diploid human cells.
The article supporting this statement is
www.ncbi.nlm.nih.gov/pmc/articles/PMC316649/
If you can provide the article claiming that leading strand have overhang, we will gladly want to look upon it and if your statement is true, we will surely amend the video.
Thank you
@@EasyPeasyLearning These are two very concepts. Telomere elongation happens just after DNA replication, so strictly speaking the leading and lagging strands do not appear as shown in the video. the newly synthesized leading strand is in complex with its parental strand, and this duplex consists of equal length strands prior to the involvement of telomorase. The newly synthesized lagging strand is similarly in complex with its parental strand, but here the parental strand is longer than the newly synthesized strand (i.e. there is overhang). Instead of labeling the strands in these duplexes as lagging and leading strands, it's better to follow literature convention and name them either 3' and 5' strand or G-strand and C-strand. Alternatively, the strands in the video could be labeled parental strand and newly synthesized lagging strand, as that is the pairing shown. The parental strand is then of course the longer G-rich strand strand ending in 3'.
So the concept that the lagging strand has a longer overhang compared to the leading strand is true, but that refers to the duplex of the lagging strand and its template compared to the leading strand and its template. It does not refer to the overhang between two strands in duplex as presented in the video. This confusion likely resulted from mislabeling these strands as leading and lagging, as discussed before. See this image for a schematic view:
www.cell.com/fulltext/S0092-8674(09)00897-6
Thank you very much for providing the information. We will definitely look into it and correct everything accordingly. We appreciate your support and feedback.
Why is the lagging strand longer than leading strand?
Lagging strand is longer to make a knot at the end of a chromosome so that the Dnase enzymes can't degrade it if its open. It is also longer then the leading strand so the telomere depletion would not affect the real Gene's present on the chromosome for a certain period of time.
@@EasyPeasyLearning but how can the lagging strand be longer if the last okazaki fragment can not be constructed?
Hi Tony, This article will help you understand it.
www.nature.com/scitable/topicpage/telomeres-of-human-chromosomes-21041/
www.intechopen.com/chapters/41797
@@EasyPeasyLearning Your source says the leading strand is longer
"Thus, as the replication fork moves along the chromosome, one of the two daughter strands is synthesized continuously. The other daughter strand, known as the lagging strand, is synthesized discontinuously in short fragments known as Okazaki fragments, each of which has its own RNA primer. The RNA primers are subsequently degraded, and the gaps between the Okazaki fragments are then filled in by the DNA repair machinery. A problem arises at the end of the chromosome, however, because the DNA repair machinery is unable to repair the gap left by the terminal RNA primer. Consequently, the new DNA molecule is shorter than the parent DNA molecule by at least the length of one RNA primer. Without a solution to this end-replication problem, chromosomes would progressively shorten over many cell divisions, a process that would bring about catastrophic consequences."
Why we have T in templete in Telomerase it must be U because of RNA template?…
Hi Rayan, yes you are right that was a mistake. Thank you for pointing it out
So you mean that the more a person gets old, the more telomerase gets shorter??
why no subtitles
Hi there, the subtitles are added to the video, thank you for your comment.
Lemon squeezy
😃 😃
Do not understanding the loop
All ur videos r full of error
How does telormaze enzymes restore telormeres
Thank you
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