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Translationally Controlled Tumor Protein (TCTP) controls growth by regulating the G1/S transition during cell cycle progression. Our genetic interaction studies show that TCTP fulfills this role by interacting with CSN4, a subunit of the COP9 Signalosome complex, known to influence CULLIN-RING ubiquitin ligases activity by controlling CULLIN (CUL) neddylation status. In agreement with these data, downregulation of  CSN4  in  Arabidopsis  and in tobacco cells leads to delayed G1/S transition comparable to that observed when  TCTP  is downregulated. Loss-of-function of  AtTCTP  leads to increased fraction of deneddylated CUL1, suggesting that AtTCTP interferes negatively with COP9 function. Similar defects in cell proliferation and CUL1 neddylation status were observed in  Drosophila  knockdown for  dCSN4  or  dTCTP , respectively, demonstrating a conserved mechanism between plants and animals. Together, our data show that CSN4 is the missing factor linking TCTP to the control of cell cycle progression and cell proliferation during organ development and open perspectives towards understanding TCTP’s role in organ development and disorders associated with TCTP miss-expression.

TCTP and CSN4 control cell cycle progression and development by regulating CULLIN1 neddylation in plants and animals