Transcriptional gene silencing (TGS) #26804
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How about 'GO:1902795 siRNA-mediated facultative heterochromatin formation'? (based on the text you cite from the intro) However according to our documentation, hirA is rather involved in 'GO:0045815 transcriptional initiation-coupled chromatin remodeling' and 'GO:0140673 transcriptional elongation-coupled chromatin remodeling' This seems consistent with the data in Fig 5 "Asf1 and SHREC Promote Nucleosome Occupancy at Heterochromatic Loci" |
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@ValWood We moved away from the (P)TSG terminology because it's used inconsistently in the literature, often as a tool to silence genes experimentally. This is why it's a synonym of the very high level term 'heterochromatin formation', different papers use "TGS" for different mechanisms. |
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In the context it is used in the heterochromatin it is used as shorthand for "heterochromatic transcriptional gene silencing" See for example: and also review Also we still have Another issue is that with the current arrangement "heterochromatin assembly" is a descendant of "gene expression", but heterochromatin assembly at the centromere isn't regulating gene expression. Perhaps heterochromatic gene silencing works better as a synonym of facultative heterochromatin formation? But the transcriptional gene silencing seems to be more about histone deacetylation and nucleosome occupancy. it isn't referring to all of the heterochromatin formation machinery although they work in parallel. I have some more papers to read today.... |
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I just read your first comment. I sort of agree, but I feel that ii) the syonym "transcriptional gene silencing/post transcriptional gene silencing" is on the wrong term |
HIRA is involved in silencing heterochromatic loci (Greenall et al., 2006; Kaufman et al., 1998; Sharp et al., 2001; Ye et al., 2007). |
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Seems to be about promoting nucleosome occupancy |
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This paper also implies quite a difference: The model: |
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Dear Val and Pascale,
I will get back to you both by the end of the weekend when I'll have read
the papers and other relevant literature in detail..
Essentially, it appears to me that the molecular phenotypes described in
these papers intersect with failing cellular mechanisms to cope with
transcripts emanating from cryptic (not selected for by evolation) RNA
polymerase II transcription initiation sites that are revealed when
nucleosome / chromatin assembly fails.
However there is more to this, I believe the results also touch on the idea
that heterochromatin machinery is not only transcription repressive, but,
under some conditions, at some types of gene promoters it actually
activates transcription.
Best, Colin
.
…On Wed, Jan 17, 2024 at 7:02 AM pgaudet ***@***.***> wrote:
How about 'GO:1902795 siRNA-mediated facultative heterochromatin
formation'?
However according to our documentation, hirA is rather involved in
'GO:0045815 transcriptional initiation-coupled chromatin remodeling' and
'GO:0140673 transcriptional elongation-coupled chromatin remodeling'
https://docs.google.com/presentation/d/15fDBhmO54zSJms25aV5nX3kgSwsHMnWgdSuPdo-ukyw/edit#slide=id.gf4888089cb_0_0
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On 18/01/2024 10:44, colinlog wrote:
Dear Val and Pascale,
I will get back to you both by the end of the weekend when I'll have read
the papers and other relevant literature in detail..
Essentially, it appears to me that the molecular phenotypes described in
these papers intersect with failing cellular mechanisms to cope with
transcripts emanating from cryptic (not selected for by evolation) RNA
polymerase II transcription initiation sites that are revealed when
nucleosome / chromatin assembly fails.
Hi Colin,
I think you are right here. I have been reading chromatin appears all
week and it's so complicated!
RE TGS, I think now that this is 2 things, it is really broader then
heterochromatin assembly (heterochromatin assembly plus degradation),
and I think you are correct about the cryptic transcripts but I'm
finding it all difficult to separate all of the different pathways.
For the pathway described as TGS this is useful
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3035992/
Re the surveillance machinery I read a paper
https://europepmc.org/article/MED/21892171 which showed that deletion of
RNA surveillance component Mlo3 (S.c YRA1) can partially rescue
deletion of essential RNAi components dcr1delta - but presumably this
is just somehow bypassing the RNAi pathway ... I can't figure out how !
However there is more to this, I believe the results also touch on the
idea
that heterochromatin machinery is not only transcription repressive, but,
under some conditions, at some types of gene promoters it actually
activates transcription.
Well transcription is required for heterochromatin assembly (which
presumably occurs in S-phase to establish the heterochromatin?)
There are so many considerations I just can't work out how everything
fits together in a universal model....
I hope you can enlighten!
Val
… Best, Colin
.
On Wed, Jan 17, 2024 at 7:02 AM pgaudet ***@***.***> wrote:
> How about 'GO:1902795 siRNA-mediated facultative heterochromatin
> formation'?
>
> However according to our documentation, hirA is rather involved in
> 'GO:0045815 transcriptional initiation-coupled chromatin remodeling'
and
> 'GO:0140673 transcriptional elongation-coupled chromatin remodeling'
>
>
https://docs.google.com/presentation/d/15fDBhmO54zSJms25aV5nX3kgSwsHMnWgdSuPdo-ukyw/edit#slide=id.gf4888089cb_0_0
>
> —
> Reply to this email directly, view it on GitHub
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<div class="moz-cite-prefix">On 18/01/2024 10:44, colinlog wrote:<br>
</div>
<blockquote type="cite" ***@***.***">
Dear Val and Pascale,
<br>
I will get back to you both by the end of the weekend when I'll
have read
<br>
the papers and other relevant literature in detail..
<br>
Essentially, it appears to me that the molecular phenotypes
described in
<br>
these papers intersect with failing cellular mechanisms to cope
with
<br>
transcripts emanating from cryptic (not selected for by evolation)
RNA
<br>
polymerase II transcription initiation sites that are revealed
when
<br>
nucleosome / chromatin assembly fails.
<br>
</blockquote>
<p><br>
</p>
<p>Hi Colin,</p>
<p>I think you are right here. I have been reading chromatin appears
all week and it's so complicated! <br>
</p>
<p>RE TGS, I think now that this is 2 things, it is really broader
then heterochromatin assembly (heterochromatin assembly plus
degradation), and I think you are correct about the cryptic
transcripts but I'm finding it all difficult to separate all of
the different pathways.</p>
<p>For the pathway described as TGS this is useful
<a class="moz-txt-link-freetext" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3035992/">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3035992/</a></p>
<p></p>
<p>Re the surveillance machinery I read a paper
<a class="moz-txt-link-freetext" href="https://europepmc.org/article/MED/21892171">https://europepmc.org/article/MED/21892171</a> which showed that
deletion of RNA surveillance component Mlo3 (S.c YRA1) can
partially rescue deletion of essential RNAi components dcr1delta
- but presumably this is just somehow bypassing the RNAi pathway
... I can't figure out how !<br>
</p>
<p><br>
</p>
<blockquote type="cite" ***@***.***">However
there is more to this, I believe the results also touch on the
idea
<br>
that heterochromatin machinery is not only transcription
repressive, but,
<br>
under some conditions, at some types of gene promoters it actually
<br>
activates transcription.
<br>
</blockquote>
<p>Well transcription is required for heterochromatin assembly
(which presumably occurs in S-phase to establish the
heterochromatin?) <br>
</p>
<p>There are so many considerations I just can't work out how
everything fits together in a universal model.... <br>
</p>
<p>I hope you can enlighten!</p>
<p><br>
</p>
<p>Val<br>
</p>
<p><br>
</p>
<p><br>
</p>
<blockquote type="cite" ***@***.***">Best,
Colin
<br>
.
<br>
<br>
On Wed, Jan 17, 2024 at 7:02 AM pgaudet ***@***.***> wrote:
<br>
<br>
> How about 'GO:1902795 siRNA-mediated facultative
heterochromatin
<br>
> formation'?
<br>
>
<br>
> However according to our documentation, hirA is rather
involved in
<br>
> 'GO:0045815 transcriptional initiation-coupled chromatin
remodeling' and
<br>
> 'GO:0140673 transcriptional elongation-coupled chromatin
remodeling'
<br>
>
<br>
>
<a class="moz-txt-link-freetext" href="https://docs.google.com/presentation/d/15fDBhmO54zSJms25aV5nX3kgSwsHMnWgdSuPdo-ukyw/edit#slide=id.gf4888089cb_0_0">https://docs.google.com/presentation/d/15fDBhmO54zSJms25aV5nX3kgSwsHMnWgdSuPdo-ukyw/edit#slide=id.gf4888089cb_0_0</a><br>
>
<br>
> —
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> Reply to this email directly, view it on GitHub
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Dear Val,
I am afraid I have not been gotten to this during the weekend because I am
still not done grading 20 x 175 exam questions and nor reviewing 16 large
grants for the Dutch research organisation, writing the book chater that I
promised a close colleague to have written by February 1st and preparing
for the management meetings I must attend sinds January 1st.
May I ask therefore delay this discussion to Friday afternoon during the
TXN work group session?
Colin
|
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No hurry for me. I don't think you will be through this list by Friday!
v
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I read quite a few papers today that refer to "Transcriptional gene silencing (TGS)
This used to be an independent term, but it is now a synonym of heterochromatin assembly, but it seems narrower.
e.g.
PMID:21211723
"Clr4 is required for both TGS and cis-PTGS of heterochromatic loci (Noma et al., 2004). Transcripts that escape heterochromatic TGS are processed into siRNAs by RNAi machinery. asf1-1 and HIRA mutants only affect TGS and not cis-PTGS. Indeed, we observed increased levels of siRNAs in asf1-1 and HIRA mutants (Figure 1E), revealing that dg/dh repeats are derepressed in these mutants but transcripts are not accumulating due to their degradation by RNAi."
is this synonym on the correct term, is there another term that I should be using? it's definitely narrower than "heterochromatin assembly"
I'll add the other references tomorrow
v
@pgaudet
@colinlog
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