Abstract
Cell migration is a key process in health and disease. In the last decade an increasing attention is given to chromatin organization in migrating cells. In various types of cells induction of migration leads to a global increase in heterochromatin levels. Heterochromatin is required for optimal cell migration capabilities, since various interventions with heterochromatin formation impeded the migration rate of numerous cell types. Heterochromatin supports the migration process by affecting both the mechanical properties of the nucleus as well as the genetic processes taking place within it. Increased heterochromatin levels elevate nuclear rigidity in a manner that allows faster cell migration in 3D environments. Condensed chromatin and a more rigid nucleus may increase nuclear durability to shear stress and prevent DNA damage during the migration process. In addition, heterochromatin reorganization in migrating cells is important for induction of migration-specific transcriptional plan together with inhibition of many other unnecessary transcriptional changes. Thus, chromatin organization appears to have a key role in the cellular migration process.
Highlights
Chromatin is classically divided to euchromatin and heterochromatin
In most of the described cases the interventions with heterochromatin formation were introduced ≥24 h before induction of migration. In such cases it is challenging to assess whether migration inhibition was due to failure of the cells to increase heterochromatin levels only upon receiving migration signals or due to alterations in their basal transcriptome
Cell migration is a key process in metastasis formation in cancer
Summary
Chromatin is classically divided to euchromatin and heterochromatin. Euchromatin contains relatively open and active chromatin regions, while heterochromatin includes more condensed, gene-poor and less active chromatin regions (Carlberg and Molnár, 2019). Induction of migration in the wound healing assay led to a rapid increase in various heterochromatin markers that could be detected already 15–60 min after introducing the migration signals These markers included the histone modifications H3K9me, H3K27me, and H4K20me, a non-phosphorylated form of histone H1 and DNA methylation (Gerlitz et al, 2007; Gerlitz and Bustin, 2010; Maizels et al, 2017). In most of the described cases the interventions with heterochromatin formation (e.g., introduction of siRNA or addition of a chemical inhibitor) were introduced ≥24 h before induction of migration In such cases it is challenging to assess whether migration inhibition was due to failure of the cells to increase heterochromatin levels only upon receiving migration signals or due to alterations in their basal transcriptome.
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