ࡱ> vxu@bjbjFFZ,, $*J```` giiiiii$R:V @ ``= l``g g  `> 屾I j g0  .  | B BGenetic studies in bilateral perisylvian polymicrogyria Tsuneda, Simone Sayuri MSc.; Souza-Kols, Daniela Aguiar BSc.; Torres, Fbio Rossi Ph.D.; Secolin, Rodrigo BSc.; Maurer-Morelli, Cludia Viana Ph.D.; Guerreiro, Marilisa Mantovani M.D. Ph.D.; Cendes, Fernando M.D. Ph.D.; Lopes-Cendes, Iscia M.D. Ph.D. CInAPCe Program MRC - http://www.cinapce.org.br/pesquisador.php?id_pesq=42 1 Departament of Medical Genetics; 2 Departament of Neurology, Faculty of Medical Sciences, University of Campinas UNICAMP, Campinas, SP, BRAZIL. Rationale: Polymicrogyria is a malformation of cortical development characterised by multiple small gyri with abnormal cortical lamination. In bilateral perisylvian polymicrogyria (BPP), the cerebral cortex on the border and in the depth of Sylvian fissures is thickened and abnormally infolded, more vertically oriented and, in some cases, extending more posterior up to the parietal lobes. Approximately 28 familial cases of BPP have been described, from which 75% are compatible with an X-linked heritance pattern. We have recently described a candidate locus for BPP at region Xq27.1-27.3. There have been reports in the literature that mutations in the gene SRPX2 (sushi-repeat protein X-linked 2) were present in a patient with BPP and two female relatives. The SRPX2 gene is localized in the most centromeric limits of the candidate locus we described for BPP on the X chromosome. Objective: To perform mutation screening in the SRPX2 gene in patients with BPP. Methods: Total genomic DNA obtained from 31 patients with BPP and normal controls was used as template for polymerase chain reactions (PCR) with primers for each exon sequence of the SRPX2 gene. The amplified fragments were submitted to DHPLC analysis and all chromatographic patterns were automated sequenced. Results: Chromatography showed a different pattern of retention time in fragments of exon 1 from 2 patients of different families. Sequencing analysis revealed a substitution of a guanine by a cytosine at the base position 82 of the exon.  SHAPE \* MERGEFORMAT  Figure 1: Chromatography analysis showing the pattern of retention of the patient (above) and a control (below).  Figure 2: Sequencing analysis that revealed the mutation. Conclusion: Our results are partial and are still under study. As the base substitution occurs in a portion of the gene that is not translated, there is a possibility that it does not cause a pathogenic change. Financial support: FAPESP 78   9 ; P Q R S ! λ~ume]~uem]RhjkhGmH sH hl mH sH h"PmH sH hGmH sH hGH*mH sH hjkhGH*mH sH h`h`CJaJmHsHh`hGmHsHh`h`mHsHh`CJaJmHsHh`hGCJaJmHsHhG hGhGhjkhG:CJOJQJaJhxt:CJOJQJaJhG:CJOJQJaJ8: ; ! " )*8$a$gd`gdG$a$gdxt! 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