# Arabidopsis Plastid-RNA Polymerase RPOTp Is Involved in Abiotic Stress Tolerance
## 3 Discussion
[54] found that most of the nuclear genes that encode different plastid transcriptional machinery components, including _RPOTp_ and _RPOTmp_, were down-regulated in Arabidopsis seedlings exposed to ABA. This expressive effect of ABA on plastid gene expression could be mediated by alarmone guanosine-30-50-bisdiphosphate (ppGpp), which accumulates in chloroplasts in response to abiotic stress, and to ABA, jasmonate or ethylene hormones [55; 56]. ppGpp binds to the \(\beta^{\prime}\)-subunit of PEP, and inhibits the transcription that depends on this RNA polymerase. There is no evidence that ppGpp could repress RPOTp activity [56]. Therefore, _RPOTp_ expression could be repressed by externally applying ABA through signaling to the nucleus, perhaps via PP2C and sucrose non fermenting protein-related kinases 2 (SnRK2) proteins, this being the pathway required for the expression of the enzymes that synthesize ppGpp [55]. Alternatively, _RPOTp_ could be indirectly repressed by retrograde signal/s from chloroplasts to the nucleus, produced in response to ABA (e.g., ROS accumulating in response to reduced photosynthetic activity promoted by ABA [57]). Our results show that the nuclear-photosynthesis gene _LHCB1_, a classic marker of plastid retrograde signaling, was down-regulated in salt-grown Col-0 seedlings. This falls in line with the reduced expression of Arabidopsis nuclear-photosynthetic genes reported by [PERSON] et al. [58] under similar stress conditions. Therefore, these findings indicate that salinity could activate chloroplast-to-nucleus signaling, and repress _LHCB1_, which occurs in response to chloroplast biogenesis inhibitor NF. Along these lines, we found that _RPOTp_ transcripts accumulated when chloroplast biogenesis was blocked by NF. Thus changes in _RPOTp_ gene expression under salt stress, like that of _LHCB1_, may also be due to plastid-to-nucleus retrograde signaling, but likely take place through an ABA-independent mechanism, because _RPOTp_ expression was not induced by ABA. Accordingly, osmotic stress can alter nuclear transcription via ABA-independent signaling pathways [59]. The perturbation of chloroplast development by mutations can also increase _RPOTp_ expression. Accordingly, genes _RPOTp_ and _RPOTm_ were overexpressed in the leaves of the _albostrians_ mutant of barley that lacks chloroplast translation [19]. We previously reported _RPOTp_ up-regulation in Arabidopsis _mterf_ mutants defective in chloroplast development [42; 49; 60; 61]. Furthermore, the results by [PERSON] et al. [62] suggest that NEP function might be reactivated when PEP activity is altered by mutations. The results discussed herein point out the existence of a rescue or compensatory mechanism triggered by impaired chloroplast function, which would lead to enhanced NEP transcript levels. GUN1 might be an important component of the NEP-dependent compensatory mechanism, because [PERSON] et al. [63] recently found that GUN1 physically interacts with RPOTp and promotes its activity when PEP function is impaired. Our results, and those of [PERSON] et al. [50], suggest that such a mechanism would also act in wild-type plants to help them cope with adverse environmental stimuli, like salt and heat stress. Notwithstanding, further research is required to better understand the mechanisms involved in reprogramming nuclear and plastid gene expressions in order to adapt chloroplast function and plant activity to salinity and other abiotic stresses.