Mammalian DNA methyltransferase 1 (DNMT1) is essential for maintaining DNA 
methylation patterns after cell division. Disruption of DNMT1 catalytic activity 
results in whole genome cytosine demethylation of CpG dinucleotides, promoting 
severe dysfunctions in somatic cells and during embryonic development. While 
these observations indicate that DNMT1-dependent DNA methylation is required for 
proper cell function, the possibility that DNMT1 has a role independent of its 
catalytic activity is a matter of controversy. Here, we provide evidence that 
DNMT1 can support cell functions that do not require the C-terminal catalytic 
domain. We report that PCNA and DMAP1 domains in the N-terminal region of DNMT1 
are sufficient to modulate E-cadherin expression in the absence of noticeable 
changes in DNA methylation patterns in the gene promoters involved. Changes in 
E-cadherin expression are directly associated with regulation of 
β-catenin-dependent transcription. Present evidence suggests that the DNMT1 acts 
on E-cadherin expression through its direct interaction with the E-cadherin 
transcriptional repressor SNAIL1.