Thus, many RPs may have distinct functions, besides their involvement in ribosome formation, which are currently unknown. Investigating these unknown functions of RPs using animal models is vital for understanding the role of ribosomal proteins in human diseases. L11 is one such RP proposed to have a dual physiological role; it is thought to participate in ribosomal assembly and in regulation of p53 activity. Studies in human cell lines have demonstrated that L11 binds to MDM2, MLN4924 prevents MDM2-mediated p53 ubiquitination and degradation, stabilizes and activates p53, and induces cell cycle arrest. Overexpression of L11 or actinomycin D-induced ribosomal stress increases this L11MDM2 interaction and subsequent p53 stabilization. The majority of p53 mutations are missense and found within the sequence-specific DNA-binding domain. Codon 273 is one of the most frequently mutated sites. The human mutant p53, which has the most common substitution , has been shown to have both dominantnegative and gain-of-function properties. Unlike most tumor-derived mutant p53 proteins, p53 retains partial sequence-specific DNA-binding and transcriptional activation functions. In addition, p53 has also been reported to interact with and activate topoisomerase I to induce genomic instability and to promote the reassociation of singlestranded RNA or DNA to a double-stranded form. We attribute this high discovery rate to several factors. First, some of the noted phenotypes would not have been detected using standard morphological criteria, including MOs with defects in lipid metabolism and vascular function. Second, we believe the secretome is enriched for key genes involved in regulatory and signaling function and will be more likely to elicit phenotypes with regional or ‘specific’ defects. Third, translational blocking MOs are able to target both maternal and zygotic messages, suggesting some functions can be uncovered using MOs that would not have been detected using standard mutagenesis approaches. Finally, the ability of MOs to elicit a full range of phenotypes due to altered dosing may identify hypomorphic-like phenotypes that would be too difficult to analyze from a strong, near-null allele. The probability that a typical infective generates a local epidemic is computed by using a branching process approximation for the initial stages of the epidemic, and equating ‘epidemic’ with the event that the branching process does not become extinct. Applying OPI resulted in 98 non-redundant clusters derived from gene ontologies highly enriched for processes such as glycolysis or protein synthesis, or for cellular components such as the proteosome core complex. Several investigators have reported real-time PCR-based fluorescence assays for detection of C. pneumoniae. The TaqMan system described in this report incorporated a real-time format in which amplification and detection are accomplished simultaneously.