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In these ~300 iPSC clones we identified 213 genes including known pluripotency genes, such as Nr5a1, Klf5, mir205 (Table S1).

By sequencing the exons of the three hiPSC-ASPM cell clones, we identified a heterozygous mutation at 9,910 C→T ln exon 25 that introduced a premature stop codon and a homozygous mutation at 7,684 A→G in exon 18 that produced a S2562G missense mutation, which is consistent with previously reported Aspm mutations in primary microcephaly patients (Bond et al., 2003) (Fig. S3B).

Among these clones, we identified the GsbN protein as a potential EN-interacting protein.

Specifically, from a total of 137 sequenced clones, we identified 19 unique trypsin-like serine protease sequences, and significantly, the male accessory gland yielded a single transcript that was not found in the other male tissues nor in any tissue from females (sequence #5, Table 2).

From these clones we identified 2482 small RNAs having insert lengths between 12 nt and 39 nt.

Of the 358 sequenced RAL-646 clones, we identified six and seven clones corresponding to opa31 and opa32 alleles, respectively.

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By using two phenotypically different resistant potato clones we identify several transcripts and proteins that only show increased expression or abundance in both incompatible potato clones that are potentially involved in resistance.

Through positional cloning we identified fukutin, the gene responsible for FCMD (13).

Using full-length cloning, we identified 47 novel full-length rhesus macaque KIRs, substantially increasing the library of known sequences.

Through map-based cloning, we identified a class IV HD-ZIP TF as the candidate gene for CsGL3.

During the analysis of EST sequences near the initial clone, we identified a second gene, SAMD9L, which is located 12740 bp distal to SAMD9.

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