Abstract
Plastid gene expression (PGE) is crucial for plant development and acclimation to various environmental stress conditions. Members of the “mitochondrial transcription termination factor” (mTERF) family, which are present in both metazoans and plants, are involved in organellar gene expression. Arabidopsis thaliana contains 35 mTERF proteins, of which mTERF10, mTERF11, and mTERF12 were previously assigned to the “chloroplast-associated” group. Here, we show that all three are localized to chloroplast nucleoids, which are associated with PGE. Knock-down of MTERF10, MTERF11, or MTERF12 has no overt phenotypic effect under normal growth conditions. However, in silico analysis of MTERF10, -11, and -12 expression levels points to a possible involvement of mTERF10 and mTERF11 in responses to abiotic stress. Exposing mutant lines for 7 days to moderate heat (30°C) or light stress (400 μmol photons m−2 s−1) fails to induce a phenotype in mterf mutant lines. However, growth on MS medium supplemented with NaCl reveals that overexpression of MTERF11 results in higher salt tolerance. Conversely, mterf10 mutants are hypersensitive to salt stress, while plants that modestly overexpress MTERF10 are markedly less susceptible. Furthermore, MTERF10 overexpression leads to enhanced germination and growth on MS medium supplemented with ABA. These findings point to an involvement of mTERF10 in salt tolerance, possibly through an ABA-mediated mechanism. Thus, characterization of an increasing number of plant mTERF proteins reveals their roles in the response, tolerance and acclimation to different abiotic stresses.
Highlights
Chloroplasts are of cyanobacterial origin (Raven and Allen, 2003) and harbor nowadays a reduced genome that mainly encodes proteins involved in photosynthesis and plastid gene expression (PGE)
The mitochondrial transcription termination factor (mTERF) proteins that have been investigated in more detail are members of the “chloroplast” cluster and the “mitochondrial” cluster
The maize homologs of Arabidopsis mTERFs-2, -3, -4, -5, -7, -9, -16, and -27 were identified in enriched maize nucleoids (Majeran et al, 2012) and Arabidopsis mTERF8 was found in preparations of the plastid transcriptionally active chromosome which is related to the nucleoid (Pfalz and Pfannschmidt, 2013)
Summary
Chloroplasts are of cyanobacterial origin (Raven and Allen, 2003) and harbor nowadays a reduced genome that mainly encodes proteins involved in photosynthesis and plastid gene expression (PGE). PGE is crucial for plant development and photosynthesis, but its regulation is only partially understood This is largely because, plastids still display characteristics of a prokaryoticlike structure of their genome, their gene expression machinery is much more elaborated compared to that of their cyanobacterial ancestor (reviewed in: Liere et al, 2011). The nucleus-encoded proteins of the mitochondrial transcription termination factor (mTERF) family regulate mitochondrial and PGE at diverse levels (Kleine and Leister, 2015). Knock-out of Mterf in mice leads to embryonic lethality (Park et al, 2007), and conditional knockout of Mterf in the heart has identified a novel role for its protein product in the biogenesis of metazoan mitochondrial ribosomes (Wredenberg et al, 2013). While the function for mTERF2 remains to be clarified, the remainder of the mammalian mTERFs do not support transcription termination, as it is suggested by their notation, but seem to take part in antisense transcription termination and ribosome biogenesis
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.