Citrus is the main fruit tree crop in the world and therefore has a tremendous economical, social and cultural impact in our society. In recent years, our knowledge on plant reproductive biology has increased considerably mostly because of the work developed in model plants. However, the information generated in these species cannot always be applied to citrus, predominantly because citrus is a perennial tree crop that exhibits a very peculiar and unusual reproductive biology. Regulation of fruit growth and development in citrus is an intricate phenomenon depending upon many internal and external factors that may operate both sequentially and simultaneously. The elements and mechanisms whereby endogenous and environmental stimuli affect fruit growth are being interpreted and this knowledge may help to provide tools that allow optimizing production and fruit with enhanced nutritional value, the ultimate goal of the Citrus Industry. This article will review the progress that has taken place in the physiology of citrus fruiting during recent years and present the current status of major research topics in this area.

Cells respond to salt stress by osmolyte synthesis and by increase of K⁺ uptake and Na⁺ efflux at the plasma membrane and of Na⁺ accumulation at the vacuole. This cellular level of response has been approached by the molecular genetics of Saccharomyces cerevisiae. Two plasma membrane proteins, Sln1 and Sho1, operate as sensors for turgor loss under mild osmotic stress. They activate the Hog1 MAP kinase which induces several defence genes, including the ENA1 Na⁺-efflux pump. Hog1-mediated induction occurs by inactivation of the Sko1 repressor. High concentrations of Na⁺ activate the calcium-dependent protein phosphatase calcineurin, which induces the ENA1 gene via the positive transcription factor Hal8/Crz1/Tcn1. Vacuoles could operate as Na⁺ sensors through a Na⁺-Ca²⁺ exchange mechanism. The electrical potential of the plasma membrane is a major determinant of the uptake of toxic cations, including Na⁺, by non-specific leakage pathways. This biophysical parameter is modulated by the concerted activities of the proton pumping Pma1 ATPase and the Trk1,2 K⁺ uptake system. Both calcineurin and the protein kinase Hal4,5 modulate Trk1,2 and, indirectly, the membrane potential and salt tolerance. The limiting role of vacuolar cation accumulation in salt tolerance has been demonstrated by expression in yeast vacuoles of the bacterial antiporter NhaA.

Here we report on a lipid‐signalling pathway in plants that is downstream of phosphatidic acid and involves the Arabidopsis protein kinase, AGC2‐1, regulated by the 3′‐phosphoinositide‐dependent kinase‐1 (AtPDK1). AGC2‐1 specifically interacts with AtPDK1 through a conserved C‐terminal hydrophobic motif that leads to its phosphorylation and activation, whereas inhibition of AtPDK1 expression by RNA interference abolishes AGC2‐1 activity. Phosphatidic acid specifically binds to AtPDK1 and stimulates AGC2‐1 in an AtPDK1‐dependent manner. AtPDK1 is ubiquitously expressed in all plant tissues, whereas expression of AGC2‐1 is abundant in fast‐growing organs and dividing cells, and activated during re‐entry of cells into the cell cycle after sugar starvation‐induced G1‐phase arrest. Plant hormones, auxin and cytokinin, synergistically activate the AtPDK1‐regulated AGC2‐1 kinase, indicative of a role in growth and cell division. Cellular localisation of GFP‐AGC2‐1 fusion protein is highly dynamic in root hairs and at some stages confined to root hair tips and to nuclei. The agc2‐1 knockout mutation results in a reduction of root hair length, suggesting a role for AGC2‐1 in root hair growth and development.

The initial stages of preprotein import into chloroplasts are mediated by the receptor GTPase Toc159. In Arabidopsis thaliana, Toc159 is encoded by a small gene family: atTOC159, atTOC132, atTOC120, and atTOC90. Phylogenetic analysis suggested that at least two distinct Toc159 subtypes, characterized by atToc159 and atToc132/atToc120, exist in plants. atTOC159 was strongly expressed in young, photosynthetic tissues, whereas atTOC132 and atTOC120 were expressed at a uniformly low level and so were relatively prominent in nonphotosynthetic tissues. Based on the albino phenotype of its knockout mutant, atToc159 was previously proposed to be a receptor with specificity for photosynthetic preproteins. To elucidate the roles of the other isoforms, we characterized Arabidopsis knockout mutants for each one. None of the single mutants had strong visible phenotypes, but toc132 toc120 double homozygotes appeared similar to toc159, indicating redundancy between atToc132 and atToc120. Transgenic complementation studies confirmed this redundancy but revealed little functional overlap between atToc132/atToc120 and atToc159 or atToc90. Unlike toc159, toc132 toc120 caused structural abnormalities in root plastids. Furthermore, when proteomics and transcriptomics were used to compare toc132 with ppi1 (a receptor mutant that is specifically defective in the expression, import, and accumulation of photosynthetic proteins), major differences were observed, suggesting that atToc132 (and atToc120) has specificity for nonphotosynthetic proteins. When both atToc159 and the major isoform of the other subtype, atToc132, were absent, an embryo-lethal phenotype resulted, demonstrating the essential role of Toc159 in the import mechanism.