Cultivar-based fruit size in olive depends on different tissue and cellular processes throughout growth

In drupe fruits, in addition to fruit size, the proportions of mesocarp and endocarp tissues are critical objectives for fruit quality, crop production and management. The olive fruit is a typical drupe, with cultivars which show a wide range in both fruit size and the proportions of mesocarp and endocarp. Characterizing the roles of tissue and cellular processes in producing genetically based fruit size variability is necessary for crop improvement, as well as deepening our understanding of fruit developmental physiology. This study used microscope image analysis to evaluate cell number and size, the growth of mesocarp and endocarp tissues, and their developmental timing in producing fruit size among six olive cultivars with a large range of fruit size. We found that cultivar mesocarp and endocarp size increased linearly with fruit size, with larger sizes favoring an increasingly greater mesocarp/endocarp ratio. Within the mesocarp, cultivar-based fruit size related directly to cell number and was established soon after bloom by cell division rate. In spite of different cell division rates, all cultivars showed similar timing of cell division activity, with the majority of cells produced in the two months after bloom but, surprisingly, a substantial number of cells formed during the following 6 months. Cell expansion was high throughout fruit growth and an important factor in achieving final fruit size, but cell size did not differ among cultivars at any time. We can conclude that fruit size differences among olive cultivars are due at the tissue level to both mesocarp and endocarp sizes and at the cellular level to cell division throughout fruit growth. Furthermore, since cell size is consistent among cultivars in spite of variable cell division, it is likely that cultivar differences in cell expansion accompany those in cell division. © 2011 Elsevier B.V.This work was supported by Spanish Ministry of Science and Innovation ERDF co-financed funds [grant number AGL2009-07248].Peer Reviewe

MOESM1 of Development of in vitro enteroids derived from bovine small intestinal crypts

Additional file 1. Video projection showing Z axis-projection of an enteroid whole-mount stained to detect cell nuclei. Video projection showing Z axis-projection of an enteroid whole-mount stained to detect cell nuclei. DAPI, blue

Prion Protein and Shadoo Are Involved in Overlapping Embryonic Pathways and Trophoblastic Development

<div><p>The potential requirement of either the Prion or Shadoo protein for early mouse embryogenesis was recently suggested. However, the current data did not allow to precise the developmental process that was affected in the absence of both proteins and that led to the observed early lethal phenotype. In the present study, using various <em>Prnp</em> transgenic mouse lines and lentiviral vectors expressing shRNAs that target the Shadoo-encoding mRNA, we further demonstrate the specific requirement of at least one of these two PrP-related proteins at early developmental stages. Histological analysis reveals developmental defect of the ectoplacental cone and important hemorrhage surrounding the <em>Prnp</em>-knockout-<em>Sprn</em>-knockdown E7.5 embryos. By restricting the RNA interference to the trophoblastic cell lineages, the observed lethal phenotype could be attributed to the sole role of these proteins in this trophectoderm-derived compartment. RNAseq analysis performed on early embryos of various <em>Prnp</em> and <em>Sprn</em> genotypes indicated that the simultaneous down-regulation of these two proteins affects cell-adhesion and inflammatory pathways as well as the expression of ectoplacental-specific genes. Overall, our data provide biological clues in favor of a crucial and complementary embryonic role of the prion protein family in <em>Eutherians</em> and emphasizes the need to further evaluate its implication in normal and pathological human placenta biology.</p> </div

Histological analysis of E7.5 embryos.

<p>E7.5 embryos were fixed and stained by hematoxylin, eosin, and saffron. Top left: schematic representation of a mouse E7.5 embryo. 1,2: FVB/N <i>Prnp^KO</i> embryos. 3,4: FG12-injected FVB/N <i>Prnp^KO</i> embryos. 5–8: LS2-injected FVB/N <i>Prnp^KO</i> embryos. 3–8: embryos that were injected at the zygotic stage. 9: LS2-infected FVB/N <i>Prnp^KO</i> embryos. *: infection performed at the blastocyst stage. Interesting features include i) the size differences between injected and non-injected embryos, ii) the relatively important hemorrhagic tissue that is totally surrounding the LS2-injected FVB/N <i>Prnp^KO</i> embryos 5, 6 and 8, iii) the developmental defect of the ectoplacental cone (area surrounded using a dashed line ) of all the LS2-injected FVB/N <i>Prnp^KO</i> embryos (5–8) that even leads to its nearly complete disappearance in embryo 6 and iv) the important developmental delay and the total disorganization of the extra-embryonic ectoderm and of the ectoplacental cone of embryo 9. Scale: 250 µm. Sho: <i>Sprn</i>.</p

Effect of trophoblastic-restricted ShRNA- mediated <i>Sprn</i> knockdown on embryo resorption at E13.5.

*<p>p<0.05 (x² test) when compared to any of the other results.</p><p>These data are a compilation of at least 2 independent experiments. No statistically significant variability was observed between the analyzed litters (more than 4 for each lentiviral infections).</p

Schematic representation of the embryonic phenotype induced by the lack of PrP and Shadoo.

<p>The lethal consequence of the absence of PrP and Shadoo during early mouse embryogenesis is indicated.</p

Effect of ShRNA-mediated <i>Sprn</i> knockdown on embryo resorption at E11.5.

*<p>p<0.05 (x² test) when compared to any of the FoxL2 results and to LS2 on P10 and FVB/N genetic backgrounds.</p><p>These data are a compilation of at least 2 independent experiments. No statistically significant variability was observed between the analyzed litters (3 for P10, more than 4 for the other lentiviral infections).</p

Venn diagram of the number of differentially expressed genes.

<p>A venn diagram of the number of genes differentially expressed between <i>Prnp^KO</i>, <i>Sprn</i>^KD, <i>Prnp</i>^KO<i>Sprn</i>^KD embryos and their wild type counterparts is given at E6.5 and E7.5.</p

List of top-function clusters for differentially expressed genes in <i>Sprn</i>-knockdown embryos.

<p>Bold faced genes: upregulated genes in <i>Sprn</i>-knockdown embryos. Un-bolded genes: downregulated genes in <i>Sprn</i>-knockdown embryos.</p

Details of the tissues and cell types sequenced to generate the TxBF RNA-Seq dataset for the sheep gene expression atlas.

<p>Details of the tissues and cell types sequenced to generate the TxBF RNA-Seq dataset for the sheep gene expression atlas.</p