Registration for a live webinar on 'Precision medicine treatment for anticancer drug resistance' is now open.
See webinar detailsWe noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- DNA methylation and genome defense: N. crassa
- X-inactivation: process involving DNA methylation
- N. crassa: vegetative/sexual phases of life cycle
- N. crassa: 5S rRNA gene distribution in genome
- The zeta-eta region
- DNA methylation in N. crassa
- Initial questions
- De-novo methylation of zeta-eta region
- Repeat-induced point mutation (RIP)
- RIP produces excess TpA's
- RIP and DNA methylation: questions
- Isolation of methylated DNA with MBD-column
- Most products of RIP are relics of transposons
- Most predicted relics of RIP are methylated
- RIP and DNA methylation: answers
- RIP is an efficient genome defense mechanism
- N. crassa: multigene families and gene pairs
- RIP'd sequences and methylated sequences
- Mutations and methylation of amRIP alleles
- Repeat-induced point mutation (RIP)
- Potential DNA MTases of N. crassa
- Possible mechanisms of RIP
- How RIP'd sequences trigger DNA methylation?
- Dissection of methylation signal generated by RIP
- Induction of methylation by A:T 25-mers
- G:C inhibit methylation by A:T rich sequences
- TpA and ApT are not needed to trigger methylation
- Distamycin inhibits DNA methylation in N. crassa
- Genetic approach to elucidate DNA methylation
- Identification of dim-5
- DIM-5 trimethylates Lys9 in H3 peptides
- Potential role of histone H3 in DNA methylation
- Histone H3 Lys9 substitutions
- DIM-5 is responsible for trimethylation of H3 Lys9
- Does DIM-5 "read" (or is it just "guided")?
- H3 peptide lies in surface groove of DIM-5
- Role of histone deacetylation in DNA methylation
- Sites of modification in histone H3 N-terminal tail
- Putative N. crassa HP1
- N. crassa HP1 is required for DNA methylation
- Localization of HP1-GFP
- DNA methylation control in N. crassa: basic model
- DNA methylation/heterochromatin in RNAi mutants
- Key points
- References
Topics Covered
- Control of DNA methylation
- repeat-induced point (RIP) mutation
- relationship of chromatin modifications and DNA methylation
- mutants that eliminate DNA methylation
- roles of histone H3 methyltransferase (DIM-5) and heterochromatin protein 1 (HP1) in DNA methylation
- indications of involvement of protein acetylation, methylation and phosphorylation in mechanism of DNA methylation
- propagation of DNA methylation and the associated silenced chromatin state
Talk Citation
Selker, E. (2007, October 1). DNA methylation and genome defense in Neurospora crassa [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 27, 2024, from https://doi.org/10.69645/YXHU3176.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Eric Selker has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.