The CacyBP/SIP protein is highly expressed in brain neurons, where it localizes in somata and in neuronal processes. The role of CacyBP/SIP is not clear at present but recently it has been suggested that the interaction between CacyBP/SIP and tubulin might be important for stability of microtubules in neuronal cells. Particularly, it was found that CacyBP/SIP changes its localization in an age-dependent way. Moreover, these changes in localization are similar to those observed for tau, a well known tubulin binding protein. Since it is known that changes in localization of tau during aging are similar to those observed in tauopaties (such as Alzheimer’s disease), in this work we examined the localization and possible role of CacyBP/SIP in mouse model of tauopathy (mice overexpressing the tau protein). We found that in young tauopathic mice CacyBP/SIP and tau are mainly present in neuronal somata whereas in wild type animals both proteins are localized in somata and in neuronal processes. Moreover, the tubulin staining pattern in transgenic mice was different than in wild animals. This might suggest that translocation of tau together with CacyBP/SIP affects stability of microtubules in neuronal cells. At present we examine whether posttranslational modifi cation(s) of CacyBP/SIP, such as phosphorylation, might be responsible for the observed translocation of CacyBP/SIP during tauopathy. This work was supported by statutory funds from the Nencki Institute of Experimental Biology.
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