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Tudor staphylococcal nuclease is an evolutionarily conserved component of the programmed cell death degradome
Jens F. Sundstr?m1,9, Alena Vaculova2,9, Andrei P. Smertenko3,9, Eugene I. Savenkov1,9, Anna Golovko1,9, Elena Minina1,9, Budhi S. Tiwari1, Salvador Rodriguez-Nieto2, Andrey A. Zamyatnin, Jr1, Tuuli V?lineva4, Juha Saarikettu4, Mikko J. Frilander5, Maria F. Suarez6, Anton Zavialov7, Ulf St?hl1, Patrick J. Hussey3, Olli Silvennoinen4,8, Eva Sundberg1, Boris Zhivotovsky2 & Peter V. Bozhkov1
Programmed cell death (PCD) is executed by proteases, which cleave diverse proteins thus modulating their biochemical and cellular functions. Proteases of the caspase family and hundreds of caspase substrates constitute a major part of the PCD degradome in animals1, 2. Plants lack close homologues of caspases, but instead possess an ancestral family of cysteine proteases, metacaspases3, 4. Although metacaspases are essential for PCD5, 6, 7, their natural substrates remain unknown4, 8. Here we show that metacaspase mcII-Pa cleaves a phylogenetically conserved protein, TSN (Tudor staphylococcal nuclease), during both developmental and stress-induced PCD. TSN knockdown leads to activation of ectopic cell death during reproduction, impairing plant fertility. Surprisingly, human TSN (also known as p100 or SND1), a multifunctional regulator of gene expression9, 10, 11, 12, 13, 14, 15, is cleaved by caspase-3 during apoptosis. This cleavage impairs the ability of TSN to activate mRNA splicing, inhibits its ribonuclease activity and is important for the execution of apoptosis. Our results establish TSN as the first biological substrate of metacaspase and demonstrate that despite the divergence of plants and animals from a common ancestor about one billion years ago and their use of distinct PCD pathways, both have retained a common mechanism to compromise cell viability through the cleavage of the same substrate, TSN.
1 Department of Plant Biology and Forest Genetics, Uppsala BioCenter, Swedish University of Agricultural Sciences, Box 7080, SE-75007 Uppsala, Sweden.
2 Institute of Environmental Medicine, Karolinska Institutet, Box 210, SE-17177, Stockholm, Sweden.
3 The Integrative Cell Biology Laboratory, School of Biological and Biomedical Sciences, University of Durham, South Road, Durham DH1 3LE, UK.
4 Institute of Medical Technology, University of Tampere, FIN-33014 Tampere, Finland.
5 Institute of Biotechnology, University of Helsinki, FIN-00014 Helsinki, Finland.
6 Departamento de Biologia Molecular y Bioquimica, Facultad de Ciencias, Universidad de Malaga, Campus de Teatinos, 29071 Malaga, Spain.
7 Department of Molecular Biology, Biomedical Center, Swedish University of Agricultural Sciences, Box 590, SE-75124 Uppsala, Sweden.
8 Department of Clinical Microbiology, Tampere University Hospital, FIN-33520 Tampere, Finland.
9 These authors contributed equally to this work.
