The Influence Of AC3 Deletion On Related Factors And Signaling Pathways In The Main Olfactory Epithelium Tissue Of Mouse

The main olfactory epithelium(MOE) organization is the vital organs for mammalian olfactory signal feeling and transduction. In the MOE, olfactory signal transduction involve at least three signaling pathways: c AMP signaling pathway, inositol-1,4,5-triphosphate(IP3)signaling pathway and Hh signaling pathway, which c AMP signaling pathway is a major pathway to produce olfactory, AC3 is one of the important members of the signaling pathway.AC3 deletions damaged the c AMP signal pathway, there were anosmia, along with the ability of attack male, maternity care, learning, memory and reproductive occurred abnormalities, a significant characteristic of body is obesity. The study found that AC2, AC3,AC4 expressed in MOE tissues, however, in the case of lack AC3, whether AC2 and AC4 play correspondence compensation in olfactory signal transduction. The AC3 in olfactory neurons(OSNs) is a highly N-glycosylated protein. In MOE tissue, the expression of β3Gn T2 affect the activation and location of AC3 in nerve axons. Thus, wether AC3 deletion caused to change expression level of β3Gn T2. In MOE tissues, some olfactory nerve cells also use IP3 as olfactory transduction signaling pathway, Hh signaling pathway affects olfactory neurons growth and branching, etc., whether AC3 deletion can make IP3, Hh signaling pathway have changes, thus to affect the signal conduction of c AMP signaling pathway. These problems is still unknown so far.To explain the above mentioned problems, this experiment taked AC3 mutation(AC3-/-)mice and their wild-type(AC3+/+) littermate mice MOE organization for materials, used real-time quantitative PCR(q RT-PCR) and immunofluorescence techniques to study the following results:1. In AC3-/- mice MOE organization, three signaling molecules ac2, ac4, β3gnt2 gene level were down-regulated, and the corresponding protein expression level were also down-regulated, the expression position of AC2, AC4, β3Gn T2 did not change.2. In AC3-/- mice MOE organization, the main gene ltrp1, calm1, calm2 of IP3 signaling pathway were down-regulated, the representative protein Ca M and IP3 KA were down-regulated expression, also the sites had not changed.3. In AC3-/- mice MOE organization, The main gene ptch, smo, gli1, gli2 of Hh signaling pathway were down-regulated, representative protein PTCH, SMO immunofluorescence staining showed that the expression level were down. Meanwhile, the expression sites of PTCH not changed, but the expression sites of the SMO were changed.In summary, in MOE of AC3-deficient mouse, lack of AC3 leaded AC2, AC4, β3Gn T2 signaling molecules to down-regulated, this result indicate that AC2, AC4 had no compensation, c AMP signaling pathway is damaged, IP3 signaling pathway and Hh signaling pathway are impaired simultaneously, all of these cause AC3-deficient mouse olfactory dysfunction. These results provided a theoretical basis for us to further study olfactory dysfunction of AC3-deficient mouse.