Initial microsatellite genotyping using selected markers from the published linkage interval[22] on chromosome 1 were consistent with linkage in family F105 and F115 (see Materials and Methods and Fig. 2 for ascertainment and descriptions of families segregating SCCD).
As a result, we had 125 genes with the assigned scores ranging from 0 to 4. Recently, Harvey et al. [1] reviewed published linkage studies from years 1995 to 2006 regarding mood disorders, and reported 26 genomic regions that showed strong linkage signals to MDD.
Candidate genes for facial clefts were selected from a variety of resources, including published linkage and association studies on clefts, genome-wide scans, gene-knockout experiments in mice, studies of chromosomal rearrangements in humans, and gene expression analyses in human and mouse embryonic tissues [2], [4], [20], [21], [22], [23].
Based on the published linkage map [ 17], scaffolds were anchored and oriented into 18 linkage groups.
Linkage groups were numbered based on the comparison with published linkage maps (Okada et al. 2010).
Marker order in every LG were almost identical to that in our published linkage map [ 28].
These 21 linkage groups were assigned to their respective chromosomes, based on previously published linkage maps [ 12- 18].
However, in other published linkage maps of P. pinaster this gene was mapped in LG 7 [ 44, 61].
In all maps, chromosome 5H has the greatest length, a mean of 198 cM, consistent with previously published linkage maps.
In short, loci such as rs6897932 will not be expected to generate any linkage signals discernable in previously published linkage screens.
All the previously published linkage maps were generated based on single F1 mapping populations, and integrated linkage maps were developed in each mapping population in all four studies.
