Love the way you teach mam, I was trying to understand this concept from last week but I couldn't, but you teach so well in just 5 minutes.Now I understood it ... Thank you very much mam
Mam. The way of teaching is awesome , I was trying to clear this concept since 3 days but I was unable to clarify but now I can cleared with this so thanks alot mam
Is there a continuation of thee wonderful video. Dr Sharma, thank you very much for such a wonderful explanation of this not so easy to understand concept.
How does the concept of dominant and recessive genes fit into this? I mean if any one of the 2 genes can get inactivated then the other one will express itself. How does this explain the concept of dominant and recessive traits? Plz explain
Regarding the first example of [ Prader - Willi syndrome ] which involves (genomic imprinting of the MATERNAL copy of chromosome 15 + deletion of the PATERNAL copy of chromosome 15) ; my question is : Is monosomy 15 compatible with life in order to develop into Prader - Willi syndrome ?
If I may answer this question, then please be informed that human beings with monosomies of any of the autosomes are not known to survive. Even if it is a case of partial monosomy of chromosome 15, wherein a good part of the long arm (q arm) of this chromosome is missing/deleted, it could lead to loss of other vital genes, which may be required in double doses for survival. Thus partial monosomies in autosomes could lead to early lethality of the individual. Hence, this explains why no partial monosomics for chromosome 15 (15q deleted) or complete monosomics for the same have been found alive to date.
@@satishsasikumar Thank you so much for your answer ! It's a common knowledge that autosomal monosomies are incompatible with life ; while Turner syndrome is the only example of sex chromosome monosomy compatible with life ! Genomic imprinting - an epigenetic effect - was discovered ONLY while studying cases of UNIPARENTAL DISOMY (UPD) , which promoted the concept of silencing gene expression on a given locus from one homologous autosomal chromosome was COMPENSATED by active expression of genes on the corresponding locus of the other homologous autosomal chromosome ! Following the concept of " genomic imprinting " ; my question can be re articulated as : By theory , can a set of genes present on an imprinted autosomal chromosome belonging to ONLY one parent suffice for survival ?
Thank you Madam for your explanation on Genomic Imprinting. I noted that in your lecture (available in this video), you did not specify which genes on maternal and paternal chromosome 15 are imprinted. During the major part of your lecture, it appeared as though all the genes on chromosome 15 are imprinted. I believe it was essential for you to mention that certain/specific genes on chromosome 15 are selectively and differentially imprinted/silenced and not all the genes. As you might know, roughly 1% of the human genome are imprinted, which means only a specific number of the genes are silenced, which are distributed on many chromosomes in the cell. Since you mentioned Prader-Willi (PW) and Angelman (ANG) syndromes, it could be stated that both disorders occur due to a deletion in 15q11-13. This region is on long arm (q arm), right below the centromere of chromosome 15 which could be deleted in the paternal chromosome leading to PW in the offspring and if the same region is deleted in the maternal chromosome 15 it leads to ANG in the progeny. The genes deleted are active SNRPN, NDN in the PW and active UBE3A in ANG.
True..it's not as simple to be explained in one line.. Histone modifications are now known to modify Gene expression in varied ways..we cannot make any Golden rule as acetylation and deacetylation both can cause over and under Gene expression
This makes me realise that pathology is really easy but we make it complicated..thanks mam. Stupider med..where is your app..it’s not found in App Store?
These are just the sample lectures Dr. Pranay. The whole app is in the recording process as Dr. Preeti wants to provide you a simple yet best way to learn pathology. Approx 50 hours of pathology will be released with her app by Jan 2019.
This video deserves million views to be very honest! Thanks a lot for the clear understanding ma'am! I need your email address, if possible would you like to mention?
Very well explained madam. But it was stopped abruptly. Please post the whole video. If you want to promote the app please don't do this. It will only have negative effect.
Awesome...But histone acetylation Makes DNA active. Medicine is too complicated to keep straight. Concept you explained is still Not perfect because OLD imprints are erased in germ cells and new imprints are made gender specific. If the Imprint in maternal origin is mutated It may become active in germ cells. Same genom from Paternal is imprinted Makes the stiation worse.
True..it's not as simple to be explained in one line.. Histone modifications are now known to modify Gene expression in varied ways..we cannot make any Golden rule as acetylation and deacetylation both can cause over and under Gene expression
