A potential relationship between transposon-derived repeats (TDR) and human 
germline methylation is of biological importance since many genes are flanked by 
TDR and methylation could affect the expression of nearby genes. Furthermore, 
DNA methylation has been suggested as a global defense mechanism against genome 
instability threatened by TDR. We studied the correlation between the density of 
HapMap methyl-associated SNPs (mSNPs), a marker of germline methylation, and 
proportion of TDR. After correcting for confounding variables, we found a 
negative correlation between proportion of Alu repeats and mSNP density for 
125-1000 kb windows. Similar results were found for the most active subgroup of 
repeats. In contrast, a negative correlation between proportion of L1 repeats 
and mSNP density was found only in the larger 1000 kb windows. Using methylation 
data on germ cells (sperm) from the Human Epigenome Project, we found a lower 
proportion of Alu repeats adjacent (3-15 kb) to hypermethylated amplicons. On 
the contrary, there was a higher proportion of L1 repeats in the 3-5 kb of 
sequence flanking hypermethylated amplicons but not in the 10-15 kb flanks. Our 
data indicate a differential response to the major repeat families and that DNA 
methylation is unlikely to be a uniform global defense system against all TDR. 
It appears to play a role for the L1 subgroup, with sequences adjacent to L1 
repeats methylated in response to their proximity. In contrast, sequences 
adjacent to Alu repeats appear to be hypomethylated, arguing against a role of 
methylation in germline defense against those elements.