No description available.

No description available.

The real-time PCR assay method was used to quantify the RNA abundance of twenty-eight plastid genes in a range of tissues and developmental stages of Arabidopsis thaliana. Three groups of co-regulated genes were identified. Three trn genes (Cluster I) showed differential expression in siliques. Genes encoding components of the plastid transcription and translation apparatus, the energetic apparatus as well as two genes encoding components of the plastid protease and acetyl-CoA carboxylase, showed maximum transcript accumulation at the 2-day stage (Cluster IIA and IIB). Finally, the genes encoding components of the photosynthetic apparatus of Cluster III reached maximum transcript abundance in later stages of chloroplast development. This coordinated expression of plastid genes reflects the presence of regulatory mechanisms that modulate plastid gene expression in different plant tissues and developmental stages. We identified an Arabidopsis mutant, rpoZ191, in which a T-DNA is inserted in the RpoT;3 gene encoding the plastid-targeted phage-type NEP enzyme. The mutant displays a general reduction in growth, as well as a delay in greening and in chloroplast development. Real-time PCR analysis of plastid RNA accumulation showed that the RpoT;3 mutation caused a significant decrease in plastid transcript accumulation at the 2-day stage and a smaller inhibition at the 5-day stage. No major effects of the RpoT;3 mutation on the accumulation of plastid transcripts was observed in mature seeds and 5-day roots. Additionally, plastid transcript accumulation in mutant siliques was not significantly different from the wild-type, except for trnfM-CAU and trnW-CCA, which showed enhanced transcript levels. Taken together, these data indicate that the RpoT;3 NEP enzyme plays an important role in the overall transcription of plastid genes during the early phases of chloroplast and leaf differentiation. Furthermore, a functional RpoT;3 is required for the activation of selected nucleus-encoded plastid-localized proteins. However, the enhanced activity of RpoT;3 during the early stages of chloroplast differentiation is not due to an increase in RpoT;3 mRNA abundance. We suggest that post-transcriptional mechanisms (e.g. phosphorylation, specificity factors) activate the transcription of plastid RpoT;3 - transcribed genes during the early stages of plastid development.

The real-time PCR assay method was used to quantify the RNA abundance of twenty-eight plastid genes in a range of tissues and developmental stages of Arabidopsis thaliana. Three groups of co-regulated genes were identified. Three trn genes (Cluster I) showed differential expression in siliques. Genes encoding components of the plastid transcription and translation apparatus, the energetic apparatus as well as two genes encoding components of the plastid protease and acetyl-CoA carboxylase, showed maximum transcript accumulation at the 2-day stage (Cluster IIA and IIB). Finally, the genes encoding components of the photosynthetic apparatus of Cluster III reached maximum transcript abundance in later stages of chloroplast development. This coordinated expression of plastid genes reflects the presence of regulatory mechanisms that modulate plastid gene expression in different plant tissues and developmental stages. We identified an Arabidopsis mutant, rpoZ191, in which a T-DNA is inserted in the RpoT;3 gene encoding the plastid-targeted phage-type NEP enzyme. The mutant displays a general reduction in growth, as well as a delay in greening and in chloroplast development. Real-time PCR analysis of plastid RNA accumulation showed that the RpoT;3 mutation caused a significant decrease in plastid transcript accumulation at the 2-day stage and a smaller inhibition at the 5-day stage. No major effects of the RpoT;3 mutation on the accumulation of plastid transcripts was observed in mature seeds and 5-day roots. Additionally, plastid transcript accumulation in mutant siliques was not significantly different from the wild-type, except for trnfM-CAU and trnW-CCA, which showed enhanced transcript levels. Taken together, these data indicate that the RpoT;3 NEP enzyme plays an important role in the overall transcription of plastid genes during the early phases of chloroplast and leaf differentiation. Furthermore, a functional RpoT;3 is required for the activation of selected nucleus-encoded plastid-localized proteins. However, the enhanced activity of RpoT;3 during the early stages of chloroplast differentiation is not due to an increase in RpoT;3 mRNA abundance. We suggest that post-transcriptional mechanisms (e.g. phosphorylation, specificity factors) activate the transcription of plastid RpoT;3 - transcribed genes during the early stages of plastid development.

Univ., Diss.--München, 2005.

Köln, University, Diss., 2003.

Universiẗat, Diss., 2003--Osnabrück. / Erscheinungsjahr an der Haupttitelstelle: 2003.

No description available.

Most herbicides acting on photosynthetic electron transport are found to be inhibitors that bind to the Q<SUB>B</SUB> protein of photosystem II, which is believed to have a plastoquinone binding site. However, evidence is now available to suggest the existence of other plastoquinone binding sites within the electron-transfer chain of chloroplasts. The cytochrome <i>bf</i> complex is involved in plastoquinol oxidation (QO site) and plastoquinone reduction (QR site). Plastoquinone is also an intermediate in the electron-transfer pathway of ferredoxin-catalysed cyclic photophosphorylation. Recent evidence is available to suggest the existence of a specific ferredoxin-plastoquinone reductase (FQR) which is not associated with the cytochrome <i>bf</i> complex. A series of routine electron-transport assays have been developed to characterize the four plastoquinone-binding sites discussed above. Inhibitors of the QR site inhibited the slow phase of the electrochromic shift (P518<SUB>s</SUB>) and the re-oxidation of cytochrome <i>b</i>-563. QO site inhibitors affected the re-reduction of both cytochromes <i>f</i> and <i>b</i>-563, in addition to the attenuation of P518<SUB>s</SUB>. Cyclic electron transport systems have been set up in broken chloroplasts with either ferredoxin or 9,10-anthraquinone-2-sulphonate as cofactor. FQR inhibitors affected the former cyclic process but not the latter. Evidence was obtained to support the recent notion of the primary site of action of antimycin being at FQR rather than the QR site, which is the primary site in mitochondria. Simple analogues of antimycin such as 3,5 dihalosalicyl-N-(n-substituted) amides also inhibited the FQR. These observations indicated that the inhibitory property of antimycin is associated with the substituted aromatic moiety whilst the remaining dilactone portion provides an additional lipophilicity. The requirement of the aromatic ring for inhibitory activity was confirmed by the effects of tetrahalogenated 4-hydroxy-pyridines. These were found to act not at the QR site as reported in the literature, but at FQR. In addition to the aromatic nucleus, these FQR inhibitors required a phenolic hydroxyl group for activity. Data obtained was consistent with an obligatory, fixed stoichiometry H<SUP>+</SUP>/e<SUP>-</SUP> of three) Q cycle in the cytochrome <i>bf</i> complex, insensitive to antimycin. Kinetic evidence supported the existence of two quinone binding sites in this complex. Inhibition at one of these, QR site, by 2-alkyl quinoline N-oxide required a high degree of lipophilicity as well as the N-oxide and a ring hydroxyl group. Structural features of the inhibitors which appear to distinguish binding at the various sites include the number of redox active groups on the aromatic nucleus, the requirement for an electron withdrawing group ortho to the redox active group, and the requirement for the redox active group to carry a negative charge.

No description available.