The role of branch architecture in assimilate production and partitioning: the example of apple (Malus domestica).

Understanding the role of branch architecture in carbon production and allocation is essential to gain more insight into the complex process of assimilate partitioning in fruit trees. This mini review reports on the current knowledge of the role of branch architecture in carbohydrate production and partitioning in apple. The first-order carrier branch of apple illustrates the complexity of branch structure emerging from bud activity events and encountered in many fruit trees. Branch architecture influences carbon production by determining leaf exposure to light and by affecting leaf internal characteristics related to leaf photosynthetic capacity. The dynamics of assimilate partitioning between branch organs depends on the stage of development of sources and sinks. The sink strength of various branch organs and their relative positioning on the branch also affect partitioning. Vascular connections between branch organs determine major pathways for branch assimilate transport. We propose directions for employing a modeling approach to further elucidate the role of branch architecture on assimilate partitioning.

A dynamic model of tomato fruit growth integrating cell division, cell growth and endoreduplication.

In this study, we developed a model of tomato (Solanum lycopersicum L.) fruit growth integrating cell division, cell growth and endoreduplication. The fruit was considered as a population of cells grouped in cell classes differing in their initial cell age and cell mass. The model describes fruit growth from anthesis until maturation and covers the stages of cell division, endoreduplication and cell growth. The transition from one stage to the next was determined by predefined cell ages expressed in thermal time. Cell growth is the consequence of sugar import from a common pool of assimilates according to the source-sink concept. During most parts of fruit growth, potential cell growth rate increases with increasing cell ploidy and follows the Richards growth function. Cell division or endoreduplication occurs when cells exceed a critical threshold cell mass:ploidy ratio. The model was parameterised and calibrated for low fruit load conditions and was validated for high fruit load and various temperature conditions. Model sensitivity analysis showed that variations in final fruit size are associated with variations in parameters involved in the dynamics of cell growth and cell division. The model was able to accurately predict final cell number, cell mass and pericarp mass under various contrasting fruit load and most of the temperature conditions. The framework developed in this model opens the perspective to integrate information on molecular control of fruit cellular processes into the fruit model and to analyse gene-by-environment interaction effects on fruit growth.

Histological and molecular investigation of the basis for variation in tomato fruit size in response to fruit load and genotype.

Understanding the molecular mechanisms and cellular dynamics that cause variation in fruit size is critical for the control of fruit growth. The aim of this study was to investigate how both genotypic factors and carbohydrate limitation cause variation in fruit size. We grew a parental line (Solanum lycopersicum L.) and two inbred lines from Solanum chmielewskii (C.M.Rick et al.; D.M.Spooner et al.) producing small or large fruits under three fruit loads (FL): continuously two fruits/truss (2&2F) or five fruits/truss (5&5F) and a switch from five to two fruits/truss (5&2F) 7 days after anthesis (DAA). Final fruit size, sugar content and cell phenotypes were measured. The expression of major cell cycle genes 7 DAA was investigated using quantitative PCR. The 5&5F treatment resulted in significantly smaller fruits than the 5&2F and 2&2F treatments. In the 5&5F treatment, cell number and cell volume contributed equally to the genotypic variation in final fruit size. In the 5&2F and 2&2F treatment, cell number contributed twice as much to the genotypic variation in final fruit size than cell volume did. FL treatments resulted in only subtle variations in gene expression. Genotypic differences were detected in transcript levels of CycD3 (cyclin) and CDKB1 (cyclin-dependent-kinase), but not CycB2. Genotypic variation in fruit FW, pericarp volume and cell volume was linked to pericarp glucose and fructose content (R2=0.41, R2=0.48, R2=0.11 respectively). Genotypic variation in cell number was positively correlated with pericarp fructose content (R2=0.28). These results emphasise the role of sugar content and of the timing of assimilate supply in the variation of cell and fruit phenotypes.