Further extensive studies on ij and maternal-exception seedlings grown even in darkness show that ij-affected plastids do contain the transcripts of the plastid genes, and the relative content of the plastid DNA is maintained at the normal level (Han et al., manuscript in preparation). Briefly, additional, new transcripts are detected, and some of the normal transcripts are not found or are barely detectable. The transcripts of different genes are present from barely detectable levels up to the normal level. Also, the transcripts from individual monocistronic or polycistronic genes are differentially accumulated. Our data strongly suggest that ij-affected plastids may undergo altered processing or stability. Surprisingly, ij and maternal-exception progeny show almost identical patterns and levels of the transcripts. Therefore, the aberrant pattern of the transcripts is not correctable (by +/ij constitution) in the subsequent generation. However, aberrations of the plastid transcripts per se are not unique to the ij mutant because we found almost identical transcript patterns in the w1 mutant (Han and Coe, manuscript in preparation).
Since we found that the ij-affected plastids still maintain transcriptional activity, we feel that it is necessary to offer another possible explanation for the diverse and non-clonal expression in ij plants. White stripes on leaves of ij plants are more frequently in the margins than in any other parts of the leaves. A hypothesis of 'ribosome-loss' (Walbot and Coe, 1979) might explain the 'position-dependent' phenotypic expression of the ij plant. Once the biogenesis of the plastid ribosomes is defective, ribosomes are limited. The ribosomes 'run out' during leaf development, especially at the regions of leaves where rapid cell division and expansion occur. The clonal analysis of maize leaves (Poethig, 1984) indicates that clonal sectors in the margins of leaves are much broader than in the middle of leaves. Therefore, it is likely that 'depletion' of ribosomes could be more severe in the margins than in any other parts of leaves. Phenotypic expression of ij is predominantly noticed in the margins of the leaves.
However, it is somewhat difficult to explain the diverse genetic background-dependent phenotypes of the ij mutant by the 'ribosome-loss' hypothesis alone. Based on the data on the transcripts of the ij-affected plastids, it is reasonable to argue that the 'ribosome-loss' event might be a consequence of alterations in the plastid transcripts. Therefore, the background-dependent expression of the ij phenotypes can be paraphrased in the following way: 'white plastids', a phenotypic marker of 'ribosome-loss', are generated via the alterations in the transcripts, in a genetic background-dependent manner. It is possible that there is a temporal difference between the immediate effect of the ij gene, whatever it might be, and the phenotypic defect ('white plastid'). This possibility already has been suggested by Coe et al. (Am. J. Bot., 1988), who postulated that "the iojap defects do not arise until after a leaf differentiates". Also, the temporal dependency of the ij defect might be an explanation for the positional distribution of the maternal-exception progeny on the ear of the female parent. The maternal-exception albino seedlings are almost exclusively located in the apical region of the ear, which matures at a different time than the basal region. This implies that the defect, probably not the immediate effect, of the ij mutant could be sensitive to a temporal program during plant development.
The simplest explanation for the complex phenotypic expression of the ij mutant during plant development is that the action of ij resides in the gate of the plastids that is required for communication between two genomic compartments, nucleus and plastid. Once the communicating devices of plastids are defective or defaulted, the plastids might no longer follow the developmental processes (e.g., cell lineage). However, we found that ij-affected plastids contain the mature sizes of the nuclear encoded photosynthetic proteins and still maintain the normal level of the genomic DNA. Therefore, the defective plastids still maintain the normal transport and processing of imported nuclear products. Taking into account the fact that the aberration in the pattern and level of the plastid transcripts is persistent in the subsequent generations, there is a possibility that a 'plastid gate' (e.g., signal transduction pathway) that is necessary for temporal and spatial expression of the plastid genomes could be altered by the ij mutant. The 'developmental kinetics' (i.e., temporal difference) from the action of the ij gene to 'white plastids' (phenotypic defect) could be determined by the sensitivity or efficiency of the plastids to receive and relay the developmental signal from the cytosol or nucleus, and even by the rate of the 'ribosome-loss' process via the alteration of the transcripts. The efficiency and activity of the 'downstream' processes could be different among the different genetic backgrounds. Also, the plastids in the tissues with the prolonged growth time (e.g., the tip of the ear) and in the leaf margins showing rapid cell division and elongation are more vulnerable to the defects of the mutant.
The hypothetical, even though highly
plausible, pathway in which the ij gene might be involved could
take a pivotal role in fine-tuning the developmental switch to determine
photosynthetic tissue (mesophyll or bundle sheath cells) or nonphotosynthetic
tissue (epidermal cells) during leaf development.
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