B) Representation of glutamylation patterns found in the knockout mouse models studied here, and interpretation of the participation of the TTLL1, TTLL7 and CCP1 in their generation. Based on the immunoblot analysis shown in Fig. 2C, it can be deduced that TTLL1 is able to hyperglutamylate both, α- and β-tubulin in the absence of CCP1. By contrast, loss of CCP1 in the absence of TTLL1 does not lead to hyperglutamylation, suggesting that TTLL7 is not sufficient to generate this phenotype. In this context, our observation that hyperglutamylation of β-tubulin is abolished with TTLL7 indicates that while TTLL1 can hyperglutamylated β-tubulin, it requires prior glutamylation by TTLL7 to do so. We thus conclude that TTLL1 specifically elongates nascent glutamate chains generated by TTLL7. 