RT Journal Article SR Electronic T1 Domain model explains propagation dynamics and stability of K27 and K36 methylation landscapes JF bioRxiv FD Cold Spring Harbor Laboratory SP 729905 DO 10.1101/729905 A1 C. Alabert A1 C. Loos A1 M. Voelker-Albert A1 S. Graziano A1 I. Forné A1 N. Reveron-Gomez A1 L. Schuh A1 J. Hasenauer A1 C. Marr A1 A. Imhof A1 A. Groth YR 2019 UL http://biorxiv.org/content/early/2019/08/08/729905.abstract AB Chromatin states must be maintained during cell proliferation to uphold cellular identity and genome integrity. Inheritance of histone modifications is central in this process. However, the histone modification landscape is challenged by incorporation of new unmodified histones during each cell cycle and the principles governing heritability remain unclear. Here, we take a quantitative computational modeling approach to describes propagation of K27 and K36 methylation states. We measure combinatorial K27 and K36 methylation patterns by quantitative mass spectrometry on subsequent generations of histones. Using model comparison, we reject active global demethylation and invoke the existence of domains defined by distinct methylation endpoints. We find that K27me3 on pre-existing histones stimulates the rate of de novo K27me3 establishment, supporting a read-write mechanism in timely chromatin restoration. Finally, we provide a detailed, quantitative picture of the mutual antagonism between K27 and K37 methylation, and propose that it stabilizes epigenetic states across cell division.