Executive Order Number Twenty-Eight, July 2003

Executive order signed by Governor Thomas Vilsck

Executive Order Number Twenty-Nine, August 2003

Executive order signed by Governor Thomas Vilsck

Executive Order Number Thirty, September 2003

Executive order signed by Governor Thomas Vilsck

Executive Order Number Thirty-One, October 2003

Executive order signed by Governor Thomas Vilsck

Executive Order Number Thirty-Two, November 2003

Executive order signed by Governor Thomas Vilsck

Executive Order Number Thirty-Three, November 2003

Executive order signed by Governor Thomas Vilsck

Executive Order Number Forty-One, April 2005

Excecutive order signed by Governor Thomas Vilsck

Executive Order Number Thirty-Five, January 2004

Excecutive order signed by Governor Thomas Vilsck

Executive Order Number Thirty-Six, June 2004

Excecutive order signed by Governor Thomas Vilsck

Executive Order Number Thirty-Seven, October 2004

Excecutive order signed by Governor Thomas Vilsck

Executive Order Number Thirty-Eight, October 2004

Excecutive order signed by Governor Thomas Vilsck

Executive Order Number Thirty Nine, January 2005

Excecutive order signed by Governor Thomas Vilsck

Executive Order Number Forty, March 2005

Excecutive order signed by Governor Thomas Vilsck

X-chromosome tiling path array detection of copy number variants in patients with chromosome X-linked mental retardation

Background: Aproximately 5–10% of cases of mental retardation in males are due to copy number variations (CNV) on the X chromosome. Novel technologies, such as array comparative genomic hybridization (aCGH), may help to uncover cryptic rearrangements in X-linked mental retardation (XLMR) patients. We have constructed an X-chromosome tiling path array using bacterial artificial chromosomes (BACs) and validated it using samples with cytogenetically defined copy number changes. We have studied 54 patients with idiopathic mental retardation and 20 controls subjects. Results: Known genomic aberrations were reliably detected on the array and eight novel submicroscopic imbalances, likely causative for the mental retardation (MR) phenotype, were detected. Putatively pathogenic rearrangements included three deletions and five duplications (ranging between 82 kb to one Mb), all but two affecting genes previously known to be responsible for XLMR. Additionally, we describe different CNV regions with significant different frequencies in XLMR and control subjects (44% vs. 20%). Conclusion:This tiling path array of the human X chromosome has proven successful for the detection and characterization of known rearrangements and novel CNVs in XLMR patients.

Analysis of the multi-copy gene family FAM90A as a copy number variant in different ethnic backgrounds

Copy number variants contribute extensively to inter-individual genomic differences, but little is known about their inter-population variability and diversity. In a previous study (Bosch et al., 2007; 16:2572-2582), we reported that the primate-specific gene family FAM90A, which accounts for as many as 25 members in the human reference assembly, has expanded the number of FAM90A clusters across the hominoid lineage. Here we examined the copy number variability of FAM90A genes in 260 HapMap samples of European, African, and Asian ancestry, and showed significant inter-population differences (p<0.0001). Based on the recent study of Stranger et al. (2007; 315:848-853), we also explored the correlation between copy number variability and expression levels of the FAM90A gene family. Despite the high genomic variability, we found a low correlation between FAM90A copy number and expression levels, which could be due to the action of independent trans-acting factors. Our results show that FAM90A is highly variable in copy number between individuals and between populations. However, this variability has little impact on gene expression levels, thus highlighting the importance of genomic variability for genes located in regions containing segmental duplications.