Acetylation-mediated suppression of transcription-independent memory: bidirectional modulation of memory by acetylation.

Learning induced changes in protein acetylation, mediated by histone acetyl transferases (HATs), and the antagonistic histone deacetylases (HDACs) play a critical role in memory formation. The status of histone acetylation affects the interaction between the transcription-complex and DNA and thus re...

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Autores principales: Katja Merschbaecher, Jakob Haettig, Uli Mueller
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Publicado: Public Library of Science (PLoS) 2012
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Acceso en línea:https://doaj.org/article/318d871e23f748cc81ce4024852f72a7
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spelling oai:doaj.org-article:318d871e23f748cc81ce4024852f72a72021-11-18T07:04:57ZAcetylation-mediated suppression of transcription-independent memory: bidirectional modulation of memory by acetylation.1932-620310.1371/journal.pone.0045131https://doaj.org/article/318d871e23f748cc81ce4024852f72a72012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23028801/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Learning induced changes in protein acetylation, mediated by histone acetyl transferases (HATs), and the antagonistic histone deacetylases (HDACs) play a critical role in memory formation. The status of histone acetylation affects the interaction between the transcription-complex and DNA and thus regulates transcription-dependent processes required for long-term memory (LTM). While the majority of studies report on the role of elevated acetylation in memory facilitation, we address the impact of both, increased and decreased acetylation on formation of appetitive olfactory memory in honeybees. We show that learning-induced changes in the acetylation of histone H3 at aminoacid-positions H3K9 and H3K18 exhibit distinct and different dynamics depending on the training strength. A strong training that induces LTM leads to an immediate increase in acetylation at H3K18 that stays elevated for hours. A weak training, not sufficient to trigger LTM, causes an initial increase in acetylation at H3K18, followed by a strong reduction in acetylation at H3K18 below the control group level. Acetylation at position H3K9 is not affected by associative conditioning, indicating specific learning-induced actions on the acetylation machinery. Elevating acetylation levels by blocking HDACs after conditioning leads to an improved memory. While memory after strong training is enhanced for at least 2 days, the enhancement after weak training is restricted to 1 day. Reducing acetylation levels by blocking HAT activity after strong training leads to a suppression of transcription-dependent LTM. The memory suppression is also observed in case of weak training, which does not require transcription processes. Thus, our findings demonstrate that acetylation-mediated processes act as bidirectional regulators of memory formation that facilitate or suppress memory independent of its transcription-requirement.Katja MerschbaecherJakob HaettigUli MuellerPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 9, p e45131 (2012)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Katja Merschbaecher
Jakob Haettig
Uli Mueller
Acetylation-mediated suppression of transcription-independent memory: bidirectional modulation of memory by acetylation.
description Learning induced changes in protein acetylation, mediated by histone acetyl transferases (HATs), and the antagonistic histone deacetylases (HDACs) play a critical role in memory formation. The status of histone acetylation affects the interaction between the transcription-complex and DNA and thus regulates transcription-dependent processes required for long-term memory (LTM). While the majority of studies report on the role of elevated acetylation in memory facilitation, we address the impact of both, increased and decreased acetylation on formation of appetitive olfactory memory in honeybees. We show that learning-induced changes in the acetylation of histone H3 at aminoacid-positions H3K9 and H3K18 exhibit distinct and different dynamics depending on the training strength. A strong training that induces LTM leads to an immediate increase in acetylation at H3K18 that stays elevated for hours. A weak training, not sufficient to trigger LTM, causes an initial increase in acetylation at H3K18, followed by a strong reduction in acetylation at H3K18 below the control group level. Acetylation at position H3K9 is not affected by associative conditioning, indicating specific learning-induced actions on the acetylation machinery. Elevating acetylation levels by blocking HDACs after conditioning leads to an improved memory. While memory after strong training is enhanced for at least 2 days, the enhancement after weak training is restricted to 1 day. Reducing acetylation levels by blocking HAT activity after strong training leads to a suppression of transcription-dependent LTM. The memory suppression is also observed in case of weak training, which does not require transcription processes. Thus, our findings demonstrate that acetylation-mediated processes act as bidirectional regulators of memory formation that facilitate or suppress memory independent of its transcription-requirement.
format article
author Katja Merschbaecher
Jakob Haettig
Uli Mueller
author_facet Katja Merschbaecher
Jakob Haettig
Uli Mueller
author_sort Katja Merschbaecher
title Acetylation-mediated suppression of transcription-independent memory: bidirectional modulation of memory by acetylation.
title_short Acetylation-mediated suppression of transcription-independent memory: bidirectional modulation of memory by acetylation.
title_full Acetylation-mediated suppression of transcription-independent memory: bidirectional modulation of memory by acetylation.
title_fullStr Acetylation-mediated suppression of transcription-independent memory: bidirectional modulation of memory by acetylation.
title_full_unstemmed Acetylation-mediated suppression of transcription-independent memory: bidirectional modulation of memory by acetylation.
title_sort acetylation-mediated suppression of transcription-independent memory: bidirectional modulation of memory by acetylation.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/318d871e23f748cc81ce4024852f72a7
work_keys_str_mv AT katjamerschbaecher acetylationmediatedsuppressionoftranscriptionindependentmemorybidirectionalmodulationofmemorybyacetylation
AT jakobhaettig acetylationmediatedsuppressionoftranscriptionindependentmemorybidirectionalmodulationofmemorybyacetylation
AT ulimueller acetylationmediatedsuppressionoftranscriptionindependentmemorybidirectionalmodulationofmemorybyacetylation
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