Background : Self-incompatibility (SI) in the Solanaceae, Rosaceae and Scrophulariaceae is gametophytically controlled by a single polymorphic locus, termed the S -locus. To date, the only known S -locus product is a polymorphic ribonuclease, termed SRNase, which is secreted by stylar tissue and thought to act as a cytotoxin that degrades the RNA of incompatible pollen tubes. However, understanding how S -RNase causes S -haplotype specific inhibition of pollen tubes has been hampered by the lack of a cloned pollen S -determinant gene.

Self-incompatibility (SI) response in Brassica is initiated by haplotype-specific interactions between the pollen-borne ligand S locus protein 11/SCR and its stigmatic S receptor kinase, SRK. This binding induces autophosphorylation of SRK, which is then thought to trigger a signaling cascade that leads to self-pollen rejection. A recessive mutation of the modifier (m) gene eliminates the SI response in stigma. Positional cloning of M has revealed that it encodes a membrane-anchored cytoplasmic serine/threonine protein kinase, designated M locus protein kinase (MLPK). Transient expression of MLPK restores the ability of mm papilla cells to reject self-pollen, suggesting that MLPK is a positive mediator of Brassica SI signaling.

Expression of nuclear-encoded plastid proteins and import of those proteins into plastids are indispensable for plastid biogenesis. One possible cellular mechanism that coordinates these two essential processes is retrograde signaling from plastids to the nucleus. However, the molecular details of how this signaling occurs remain elusive. Using the plastid protein import2 mutant of Arabidopsis (Arabidopsis thaliana), which lacks the atToc159 protein import receptor, we demonstrate that the expression of photosynthesis-related nuclear genes is tightly coordinated with their import into plastids. Down-regulation of photosynthesis-related nuclear genes is also observed in mutants lacking other components of the plastid protein import apparatus. Genetic studies indicate that the coordination of plastid protein import and nuclear gene expression is independent of proposed plastid signaling pathways such as the accumulation of Mg-protoporphyrin IX and the activity of ABA INSENSITIVE4 (ABI4). Instead, it may involve GUN1 and the transcription factor AtGLK. The expression level of AtGLK1 is tightly correlated with the expression of photosynthesis-related nuclear genes in mutants defective in plastid protein import. Furthermore, the activity of GUN1 appears to down-regulate the expression of AtGLK1 when plastids are dysfunctional. Based on these data, we suggest that defects in plastid protein import generate a signal that represses photosynthesis-related nuclear genes through repression of AtGLK1 expression but not through activation of ABI4.Plastids are a diverse group of organelles that perform essential metabolic and signaling functions within all plant cells. It is generally believed that plastids originated from a unicellular photosynthetic bacterium that was taken up by a eukaryotic host cell (Dyall et al., 2004). During evolution, most of the genes encoded by the bacterial ancestor have been transferred to the host nuclear genome; for example, the plastid genome of Arabidopsis (Arabidopsis thaliana) encodes fewer than 100 open reading frames (Martin et al., 1998). Consequently, plastid biogenesis is dependent on the import of nuclear-encoded plastid proteins (Keegstra and Cline, 1999;Soll and Schleiff, 2004;Kessler and Schnell, 2006;Inaba and Schnell, 2008;Jarvis, 2008), the genes for which must be expressed at an appropriate level. For example, many of the photosynthesis-related nuclear genes that are required for chloroplast biogenesis are induced via photoreceptors, such as phytochrome, in response to light quality and quantity (Terzaghi and Cashmore, 1995), so that the photosynthesis-related proteins will be available for import into the developing chloroplasts. Other types of plastids, according to their specific metabolic functions, need other sets of nuclear-encoded proteins. Therefore, the expression of specific sets of nuclear genes and the import of their translation products are indispensable for plastid differentiation.After they have been imported into plastids, nuclear-encoded plastid proteins combi...