The significance of these 42 missing genes is not clear. The average gene length is comparable between the 2 species: 1.57 kb and 1.72 kb, for C. hominis and C. parvum, respectively. Genome comparison showed that C. hominis and buy LDN-193189 C. parvum are very similar. This high level of sequence similarity limited the ability of comparative genomics to improve annotation, identify conserved non-coding sequence elements and study gene and protein evolution [16]. More importantly, this high sequence similarity hindered better understanding of host specificity and virulence mechanisms as was anticipated from the genome projects [17]. In fact, C.

hominis and C. parvum genomes exhibit only 3-5% sequence divergence, with no large insertions, deletions or rearrangements [15]. The authors stated that the gene complements of the two species are essentially identical because the few C. parvum genes not found in C. hominis are proximal to known sequence gaps. However, uncertainty about the amount of sequence variation between C. parvum and C. hominis persists due to the incomplete status of the C. hominis genome. Nevertheless, it has been concluded that the phenotypic differences between C. hominis selleck chemicals llc and C. parvum are caused by polymorphisms in coding regions and differences in gene regulation [15, 18]. The role of this minimal genetic variability between C. hominis and C. parvum in the phenotypic differences is now much more

accessible for investigation. In fact, these genes may include hitherto valuable epidemiological Eltanexor mouse markers and previously unnoticed genetic determinants of host specificity and virulence. In addition, such markers would also serve as typing targets. The aim of this study was to survey the published C. parvum and C. hominis genomes for incomplete regions and missing genes in order to identify novel genotyping markers. These genes

are likely to contribute to the phenotypic differences between C. parvum and C. hominis and therefore might be potential genetic determinants of host tropism. Results Initial screening by Reciprocal Blast and retention of coding sequences showing a level of similarity below 10% (and supported by significant p values) identified 117 and 272 putative species-specific genes for C. hominis and C. parvum, Bcr-Abl inhibitor respectively. The majority of C. parvum putative specific genes were annotated, while C. hominis putative specific genes corresponded mainly to hypothetical proteins. Subsequently, the secondary screen decreased the number of the predicted genes to 93 and 211 genes for C. hominis and C. parvum, respectively. Initially, a subset of ten genes was selected semi-randomly with preference to annotated genes (Table 1). This subset of genes was tested experimentally by PCR in a collection of Cryptosporidium clinical isolates and reference strains (Table 2). Surprisingly, 90% (9/10) of the genes tested were present in both C. hominis and C. parvum. PCR results for Cgd2_80 and Chro.