Tbccd1, a protein related to tubulin cofactor C, is crucial for internal cell organization. It localizes at the centrosome, spindle midzone, midbody, and basal bodies of cilia. It plays roles in centrosome positioning, Golgi apparatus organization, and is associated with cytoskeletal filament formation [1,3]. Genetic models are valuable for studying Tbccd1's functions in various organisms.

In RPE-1 cells, knockdown of Tbccd1 led to centrosome dissociation from the nucleus, Golgi apparatus disorganization, larger cell size, less efficient primary cilia assembly, and slower cell migration in wound-healing assays, while major microtubule-nucleating activity was unaffected [1]. In Ectocarpus, mutations in the DIS gene encoding TBCCd1 caused loss of basal structures, with abnormalities in the germinating initial cell such as increased cell size, Golgi disorganization, microtubule network disruption, and aberrant nucleus positioning [2]. In Trypanosoma brucei, loss of Tbccd1 led to disorganization of the Golgi 'bi-lobe' architecture and loss of centriole-kinetoplast linkage [3]. In Chlamydomonas reinhardtii, Tbccd1 is required for mother-daughter centriole linkage [3,4]. In asq2 mutant cells (where ASQ2 encodes Tbccd1), there were defects in centriole number control, centriole positioning, and spindle orientation due to perturbed centriole linkage [4].

In conclusion, Tbccd1 is essential for multiple cellular processes including centrosome and Golgi apparatus positioning, centriole linkage, and cytoskeletal organization. Model-based research, especially through loss-of-function experiments, has revealed its significance in different organisms. Although no specific disease areas related to Tbccd1 KO/CKO mouse models were mentioned in the provided references, the understanding of its functions can potentially contribute to insights in relevant disease-related cell biology [1-3,6].