Table 3 Summary of the significantly associated DMRs for each PLR latency phenotype.

From: Epigenome-wide analysis identifies DNA methylation signatures associated with the infant pupillary light reflex, a candidate intermediate phenotype for autism

Latency phenotype (months)

Genomic locations (hg19)

N probes

Probes

Illumina gene annotations

Effect size (β)1

Bonf.-adjust p-value

9

chr10:74927623–74,927,863

8

cg15213114; cg04167018; cg21416602; cg25138168; cg08571229; cg04749667; cg16124546; cg12276298

FAM149B1; ECD

−0.007

7.25 × 10− 3

14

chr1:103573700–103,573,772

2

cg26436330; cg20847625

COL11A1

0.01

6.33 × 10− 4

24

chr:1045495981-45496216

3

cg18382353; cg16512882; cg15078013

C10orf25; ZNF22

−0.02

8.49 × 10− 4

9 to 14

chr3:52569053–52,569,169

3

cg18337363; cg08365687; cg13284614

NT5DC2; LOC440957

−0.009

7.35 × 10− 3

14 to 242

chr17:2699706–2,699,718

2

cg05890550; cg25373595

RAP1GAP2

0.02

6.53 × 10− 5

  1. Bonf.-adjust Bonferroni-adjusted. 1A negative effect size (-β) indicates hypermethylation associated with faster latency (for cross-sectional measurements) or latency becoming slower over time (for change scores).2This row details the topmost significant DMR to associate with 14- to 24-month latency change (see SM 4 Table 2 for a summary of all DMRs significantly associated with PLR latency).
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