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Regulation of DCC localization by HTZ-1/H2A.Z and DPY-30 does not correlate with H3K4 methylation levels.
PLoS One. 2011; 6(10):e25973.Plos

Abstract

Dosage compensation is a specialized form of gene regulation that balances sex-chromosome linked gene expression between the sexes. In C. elegans, dosage compensation is achieved by the activity of the dosage compensation complex (DCC). The DCC binds along both X chromosomes in hermaphrodites to down-regulate gene expression by half, limiting X-linked gene products to levels produced in XO males. Sequence motifs enriched on the X chromosome play an important role in targeting the DCC to the X. However, these motifs are not strictly X-specific and therefore other factors, such as the chromatin environment of the X chromosome, are likely to aid in DCC targeting. Previously, we found that loss of HTZ-1 results in partial disruption of dosage compensation localization to the X chromosomes. We wanted to know whether other chromatin components coordinated with HTZ-1 to regulate DCC localization. One candidate is DPY-30, a protein known to play a role in DCC localization. DPY-30 homologs in yeast, flies, and mammals are highly conserved members of histone H3 lysine 4 (H3K4) methyltransferase Set1/MLL complexes. Therefore, we investigated the hypothesis that the dosage compensation function of DPY-30 involves H3K4 methylation. We found that in dpy-30 animals the DCC fails to stably bind chromatin. Interestingly, of all the C. elegans homologs of Set1/MLL complex subunits, only DPY-30 is required for stable DCC binding to chromatin. Additionally, loss of H3K4 methylation does not enhance DCC mislocalization in htz-1 animals. We conclude that DPY-30 and HTZ-1 have unique functions in DCC localization, both of which are largely independent of H3K4 methylation.

Authors+Show Affiliations

Department of Molecular, University of Michigan, Ann Arbor, Michigan, United States of America.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21998734

Citation

Petty, Emily, et al. "Regulation of DCC Localization By HTZ-1/H2A.Z and DPY-30 Does Not Correlate With H3K4 Methylation Levels." PloS One, vol. 6, no. 10, 2011, pp. e25973.
Petty E, Laughlin E, Csankovszki G. Regulation of DCC localization by HTZ-1/H2A.Z and DPY-30 does not correlate with H3K4 methylation levels. PLoS ONE. 2011;6(10):e25973.
Petty, E., Laughlin, E., & Csankovszki, G. (2011). Regulation of DCC localization by HTZ-1/H2A.Z and DPY-30 does not correlate with H3K4 methylation levels. PloS One, 6(10), e25973. https://doi.org/10.1371/journal.pone.0025973
Petty E, Laughlin E, Csankovszki G. Regulation of DCC Localization By HTZ-1/H2A.Z and DPY-30 Does Not Correlate With H3K4 Methylation Levels. PLoS ONE. 2011;6(10):e25973. PubMed PMID: 21998734.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of DCC localization by HTZ-1/H2A.Z and DPY-30 does not correlate with H3K4 methylation levels. AU - Petty,Emily, AU - Laughlin,Emily, AU - Csankovszki,Györgyi, Y1 - 2011/10/05/ PY - 2011/06/09/received PY - 2011/09/14/accepted PY - 2011/10/15/entrez PY - 2011/10/15/pubmed PY - 2012/2/14/medline SP - e25973 EP - e25973 JF - PloS one JO - PLoS ONE VL - 6 IS - 10 N2 - Dosage compensation is a specialized form of gene regulation that balances sex-chromosome linked gene expression between the sexes. In C. elegans, dosage compensation is achieved by the activity of the dosage compensation complex (DCC). The DCC binds along both X chromosomes in hermaphrodites to down-regulate gene expression by half, limiting X-linked gene products to levels produced in XO males. Sequence motifs enriched on the X chromosome play an important role in targeting the DCC to the X. However, these motifs are not strictly X-specific and therefore other factors, such as the chromatin environment of the X chromosome, are likely to aid in DCC targeting. Previously, we found that loss of HTZ-1 results in partial disruption of dosage compensation localization to the X chromosomes. We wanted to know whether other chromatin components coordinated with HTZ-1 to regulate DCC localization. One candidate is DPY-30, a protein known to play a role in DCC localization. DPY-30 homologs in yeast, flies, and mammals are highly conserved members of histone H3 lysine 4 (H3K4) methyltransferase Set1/MLL complexes. Therefore, we investigated the hypothesis that the dosage compensation function of DPY-30 involves H3K4 methylation. We found that in dpy-30 animals the DCC fails to stably bind chromatin. Interestingly, of all the C. elegans homologs of Set1/MLL complex subunits, only DPY-30 is required for stable DCC binding to chromatin. Additionally, loss of H3K4 methylation does not enhance DCC mislocalization in htz-1 animals. We conclude that DPY-30 and HTZ-1 have unique functions in DCC localization, both of which are largely independent of H3K4 methylation. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/21998734/Regulation_of_DCC_localization_by_HTZ_1/H2A_Z_and_DPY_30_does_not_correlate_with_H3K4_methylation_levels_ L2 - http://dx.plos.org/10.1371/journal.pone.0025973 DB - PRIME DP - Unbound Medicine ER -