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235: Maternal H3K9 methyltransferases control aRMAE in C. elegans

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Manage episode 525420560 series 3682575
Content provided by [email protected] (Gustavo Barra) and Gustavo Barra. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by [email protected] (Gustavo Barra) and Gustavo Barra or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://podcastplayer.com/legal.

️ Episode 235: Maternal H3K9 methyltransferases control aRMAE in C. elegans

In this episode of PaperCast Base by Base, we explore Using dual-color reporters in C. elegans, the study shows maternal H3K9 methyltransferases MET-2 and SET-25 antagonistically regulate autosomal random monoallelic expression initiated in the early embryo

Study Highlights:
Dual-color fluorescent reporter alleles in C. elegans intestine cells enabled single-cell quantification of allele expression and a targeted screen for aRMAE regulators. MET-2/SETDB1, with LIN-65 and ARLE-14, acts maternally in the 8-cell E-cell to prevent monoallelic expression, while SET-25/SUV39 with HPL-2 and LIN-61 promotes allele silencing. Catalytic SET domains of both MET-2 and SET-25 are required for their opposing activities, and loss of MET-2 increases persistent but non-heritable monoallelic expression whereas loss of SET-25 causes biallelic expression. Reciprocal crosses and genetic interactions indicate these maternal H3K9 HMTs set early embryonic histone states that are propagated through somatic divisions to shape tissue-wide allele expression.

Conclusion:
Maternal MET-2 and SET-25 establish competing H3K9-related chromatin states in the early embryo that bias autosomal alleles toward persistent somatic monoallelic or biallelic expression

Music:
Enjoy the music based on this article at the end of the episode.

Reference:
Sands, B., Yun, S.R., Oshima, J. et al. Maternal histone methyltransferases antagonistically regulate autosomal random monoallelic expression (aRMAE) in C. elegans. Nat Commun (2025). https://doi.org/10.1038/s41467-025-66501-5

License:
This episode is based on an open-access article published under the Creative Commons Attribution 4.0 International License (CC BY 4.0) – https://creativecommons.org/licenses/by/4.0/

Support:
Base by Base – Stripe donations: https://donate.stripe.com/7sY4gz71B2sN3RWac5gEg00

Official website https://basebybase.com

Castos player https://basebybase.castos.com

On PaperCast Base by Base you’ll discover the latest in genomics, functional genomics, structural genomics, and proteomics.

Keywords: histone-methyltransferase, aRMAE, MET-2, SET-25, c-elegans

  continue reading

237 episodes

Artwork
iconShare
 
Manage episode 525420560 series 3682575
Content provided by [email protected] (Gustavo Barra) and Gustavo Barra. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by [email protected] (Gustavo Barra) and Gustavo Barra or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://podcastplayer.com/legal.

️ Episode 235: Maternal H3K9 methyltransferases control aRMAE in C. elegans

In this episode of PaperCast Base by Base, we explore Using dual-color reporters in C. elegans, the study shows maternal H3K9 methyltransferases MET-2 and SET-25 antagonistically regulate autosomal random monoallelic expression initiated in the early embryo

Study Highlights:
Dual-color fluorescent reporter alleles in C. elegans intestine cells enabled single-cell quantification of allele expression and a targeted screen for aRMAE regulators. MET-2/SETDB1, with LIN-65 and ARLE-14, acts maternally in the 8-cell E-cell to prevent monoallelic expression, while SET-25/SUV39 with HPL-2 and LIN-61 promotes allele silencing. Catalytic SET domains of both MET-2 and SET-25 are required for their opposing activities, and loss of MET-2 increases persistent but non-heritable monoallelic expression whereas loss of SET-25 causes biallelic expression. Reciprocal crosses and genetic interactions indicate these maternal H3K9 HMTs set early embryonic histone states that are propagated through somatic divisions to shape tissue-wide allele expression.

Conclusion:
Maternal MET-2 and SET-25 establish competing H3K9-related chromatin states in the early embryo that bias autosomal alleles toward persistent somatic monoallelic or biallelic expression

Music:
Enjoy the music based on this article at the end of the episode.

Reference:
Sands, B., Yun, S.R., Oshima, J. et al. Maternal histone methyltransferases antagonistically regulate autosomal random monoallelic expression (aRMAE) in C. elegans. Nat Commun (2025). https://doi.org/10.1038/s41467-025-66501-5

License:
This episode is based on an open-access article published under the Creative Commons Attribution 4.0 International License (CC BY 4.0) – https://creativecommons.org/licenses/by/4.0/

Support:
Base by Base – Stripe donations: https://donate.stripe.com/7sY4gz71B2sN3RWac5gEg00

Official website https://basebybase.com

Castos player https://basebybase.castos.com

On PaperCast Base by Base you’ll discover the latest in genomics, functional genomics, structural genomics, and proteomics.

Keywords: histone-methyltransferase, aRMAE, MET-2, SET-25, c-elegans

  continue reading

237 episodes

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