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The effect of translationally controlled tumour protein (TCTP) on programmed cell death in plants
VerfasserHoepflinger, Marion Christine ; Reitsamer, Johannes ; Geretschlaeger, Anja Maria ; Mehlmer, Norbert ; Tenhaken, Raimund In der Gemeinsamen Normdatei der DNB nachschlagen
Erschienen in
BMC Plant Biology, London, 2013, Jg. 13, H. 135, S. 1-9
ErschienenBioMed Central, 2013
published version
DokumenttypAufsatz in einer Zeitschrift
Schlagwörter (EN)TCTP / Programmed cell death / BAX / Tunicamycin / Unfolded protein response / Calcium / Endoplasmic reticulum / Mitochondria
URNurn:nbn:at:at-ubs:3-287 Persistent Identifier (URN)
 Das Werk ist frei verfügbar
The effect of translationally controlled tumour protein (TCTP) on programmed cell death in plants [1.26 mb]
Zusammenfassung (Englisch)

Background: Translationally controlled tumour protein (TCTP), a well known protein of the animal kingdom, was shown to be a Ca2+-binding protein with important functions in many different cellular processes (e.g. protection against stress and apoptosis, cell growth, cell cycle progression, and microtubule organization). However, only little is known about TCTP in plants. Transcript and protein levels of plant TCTPs were shown to be altered by various stress conditions (e.g. cold, salt, draught, aluminium, and pathogen infection), and Arabidopsis thaliana TCTP (AtTCTP) was described as an important regulator of growth. The aim of this study was to further characterize plant TCTP relating to one of its major functions in animals: the protection against cell death. Results: We used two different activators of programmed cell death (PCD) in plants: the mammalian pro-apoptotic protein BAX and tunicamycin, an inhibitor of glycosylation and trigger of unfolded protein response (UPR). Over-expression of AtTCTP significantly decreased cell death in tobacco leaf discs in both studies. A 45Ca overlay assay showed AtTCTP to be a Ca2+-binding protein and localization experiments revealed cytosolic distribution of AtTCTP-GFP in Arabidopsis seedlings. Conclusions: Our study showed cytoprotective effects of plant TCTP for the first time. Furthermore, we showed the ability of AtTCTP to bind to Ca2+ and its cytosolic distribution within the cell. If these results are combined, two putative modes of action can be assumed: 1) AtTCTP acts as Ca2+ sequester, preventing PCD by reducing cytosolic Ca2+ levels as described for animals. 2) AtTCTP could directly or indirectly interact with other cytosolic or membrane-bound proteins of the cell death machinery, thereby inhibiting cell death progression. As no homologous proteins of the anti-apoptotic machinery of animals were found in plants, and functional homologues still remain to be elucidated, future work will provide more insight.