City of Fairfield, Independent Auditor's Report, Basic Financial Statements and Supplementary Information, Schedule of Findings and Questioned Costs, June 30, 2004

City Audit Report

Grundy County, Independent Auditor's Reports, Basic Financial Statements and Supplementary Information, Schedule of Findings and Questioned Costs, June 30, 2004

County Audit Report

Montgomery County, Independent Auditor's Reports, Basic Financial Statements and Supplementary Information, Schedule of Findings, June 30, 2004

County Audit Report

Lee County, Independent Auditor's Reports, Basic Financial Statements and Supplementary Information, Schedule of Findings and Questioned Costs, June 30, 2004

County Audit Report

City of Central City, Independent Auditor's Reports, Basic Financial Statements and Supplementary Information, Schedule of Findings and Questioned Costs, June 30, 2003 & June 30, 2004

City Audit Report

5B Judicial District Youth Services, Independent Auditor's Reports, Basic Financial Statements, Schedule of Findings, Eight Months ended February 28, 2005 and Year ended June 30, 2004

Other Audit Reports - 28E Organizations

5B Judicial District Youth Services, Independent Auditor's Reports, Basic Financial Statements, Schedule of Findings, Eight months ended February 28, 2005 and Year Ended June 30, 2004

Other Audit Reports - 28E Organizations

Jasper County, Independent Auditor's Reports, Basic Financial Statements and Supplementary Information, Schedule of Findings and Questioned Costs, June 30, 2004

County Audit Report

Dickinson County, Independent Auditor's Reports, Basic Financial Statements and Supplementary Information, Schedule of Findings, June 30, 2004

County Audit Report

Fremont County Landfill Commission, Independent Auditor's Reports, Basic Finacial Statements and Required Supplementary Information, Schedule of Findings, June 30, 2004

Other Audit Reports - 28E Organizations

Iowa Federal Family Education Loan Program Division, Iowa College Student Aid Commission, Independent Auditor's Reports, Basic Financial Statements and Supplementary Information, June 30, 2004

State Audit Reports

Evolutionary origin and functions of retrogene introns.

Retroposed genes (retrogenes) originate via the reverse transcription of mature messenger RNAs from parental source genes and are therefore usually devoid of introns. Here, we characterize a particular set of mammalian retrogenes that acquired introns upon their emergence and thus represent rare cases of intron gain in mammals. We find that although a few retrogenes evolved introns in their coding or 3' untranslated regions (untranslated region, UTR), most introns originated together with untranslated exons in the 5' flanking regions of the retrogene insertion site. They emerged either de novo or through fusions with 5' UTR exons of host genes into which the retrogenes inserted. Generally, retrogenes with introns display high transcription levels and show broader spatial expression patterns than other retrogenes. Our experimental expression analyses of individual intron-containing retrogenes show that 5' UTR introns may indeed promote higher expression levels, at least in part through encoded regulatory elements. By contrast, 3' UTR introns may lead to downregulation of expression levels via nonsense-mediated decay mechanisms. Notably, the majority of retrogenes with introns in their 5' flanks depend on distant, sometimes bidirectional CpG dinucleotide-enriched promoters for their expression that may be recruited from other genes in the genomic vicinity. We thus propose a scenario where the acquisition of new 5' exon-intron structures was directly linked to the recruitment of distant promoters by these retrogenes, a process potentially facilitated by the presence of proto-splice sites in the genomic vicinity of retrogene insertion sites. Thus, the primary role and selective benefit of new 5' introns (and UTR exons) was probably initially to span the often substantial distances to potent CpG promoters driving retrogene transcription. Later in evolution, these introns then obtained additional regulatory roles in fine tuning retrogene expression levels. Our study provides novel insights regarding mechanisms underlying the origin of new introns, the evolutionary relevance of intron gain, and the origin of new gene promoters.

City of Carter Lake, Independent Auditor's Reports, Basic Financial Statements and Supplementary Information, Schedule of Findings, June 30, 2005

City Audit Report

City of Donnellson Independent Auditor's Report Basic Finanical Statements and Supplementary Information Schedule of Findings, June 30, 2004

Independent Auditor's Reports, Basic Financial Statements, Supplementary Information and Schedule of Findings

IRF6 is a mediator of Notch pro-differentiation and tumour suppressive function in keratinocytes.

While the pro-differentiation and tumour suppressive functions of Notch signalling in keratinocytes are well established, the underlying mechanisms remain poorly understood. We report here that interferon regulatory factor 6 (IRF6), an IRF family member with an essential role in epidermal development, is induced in differentiation through a Notch-dependent mechanism and is a primary Notch target in keratinocytes and keratinocyte-derived SCC cells. Increased IRF6 expression contributes to the impact of Notch activation on growth/differentiation-related genes, while it is not required for induction of 'canonical' Notch targets like p21(WAF1/Cip1), Hes1 and Hey1. Down-modulation of IRF6 counteracts differentiation of primary human keratinocytes in vitro and in vivo, promoting ras-induced tumour formation. The clinical relevance of these findings is illustrated by the strikingly opposite pattern of expression of Notch1 and IRF6 versus epidermal growth factor receptor in a cohort of clinical SCCs, as a function of their grade of differentiation. Thus, IRF6 is a primary Notch target in keratinocytes, which contributes to the role of this pathway in differentiation and tumour suppression.