Mottling on Sweet Cherry Fruit Is Caused by Exocarp Strain

Mottling (pale spots) is clearly visible to the naked eye in all regions of the surface in all except for yellow cultivars of sweet cherry fruit (Prunus avium L.). The objective was to characterize these spots and their distribution on the exocarp. Within the spots, anthocyanins were limited to the epidermal cell layer but, in areas immediately adjacent to the spots, anthocyanins were present in the epidermal and in the hypodermal cell layers (making these areas darker). In ‘Sam’ sweet cherries, the median length and width of a spot in the cheek region were 390 and 162 μm, respectively, and the median area was 0.053 mm2 per spot. The spatial density in the cheek region averaged 1.94 (± 0.13) spots per mm2 and the percentage of surface area covered by the spots was 12.5% (± 1.07%). Epidermal cells within a spot had slightly larger projected surface areas than those in the adjacent region and thicker cell walls. The margins of the spots did not align with the anticlinal walls of the epidermal cells. The spots’ long axes were oriented parallel with the stem/stylar scar axis, whereas the slightly elongated epidermal cells within and adjacent to the spots were orientated perpendicular to the stem/stylar scar axis. The spatial density of spots and the cumulative spot area were highest in the region of the stylar scar, intermediate in the cheek and stem cavity, and lowest in the suture region. Spot spatial density on small fruit exceeded that on larger fruit, but the areas of individual spots was smaller. When an exocarp segment was excised from the cheek of a fruit, it contracted slightly as elastic strain was released. The projected surface area of the spots and that of the whole segment decreased to a similar extent. Our data suggest that spots result from a tensional failure during Stage III development in which the anthocyanin-containing hypodermal cell layer tears (schizogenously) and separates from the epidermis. This being the case, the pale spots (mottling) can be referred to as “strain spots.”

Activation of Hypodermal Differentiation in theCaenorhabditis elegans Embryo by GATA Transcription Factors ELT-1 and ELT-3

ABSTRACT The Caenorhabditis elegans GATA transcription factor genes elt-1 and elt-3 are expressed in the embryonic hypodermis (also called the epidermis). elt-1 is expressed in precursor cells and is essential for the production of most hypodermal cells (22). elt-3 is expressed in all of the major hypodermal cells except the lateral seam cells, and expression is initiated immediately after the terminal division of precursor lineages (13). Although this expression pattern suggests a role for ELT-3 in hypodermal development, no functional studies have yet been performed. In the present paper, we show that either elt-3 or elt-1 is sufficient, when force expressed in early embryonic blastomeres, to activate a program of hypodermal differentiation even in blastomeres that are not hypodermal precursors in wild-type embryos. We have deleted the elt-3gene and shown that ELT-3 is not essential for either hypodermal cell differentiation or the viability of the organism. We showed that ELT-3 can activate hypodermal gene expression in the absence of ELT-1 and that, conversely, ELT-1 can activate hypodermal gene expression in the absence of ELT-3. Overall, the combined results of the mutant phenotypes, initial expression times, and our forced-expression experiments suggest that ELT-3 acts downstream of ELT-1 in a redundant pathway controlling hypodermal cell differentiation.

The mac1 Mutation Alters the Developmental Fate of the Hypodermal Cells and Their Cellular Progeny in the Maize Anther

In angiosperm ovules and anthers, the hypodermal cell layer provides the progenitors of meiocytes. We have previously reported that the multiple archesporial cells1 (mac1) mutation identifies a gene that plays an important role in the switch of the hypodermal cells from the vegetative pathway to the meiotic (sporogenous) pathway in maize ovules. Here we report that the mac1 mutation alters the developmental fate of the hypodermal cells of the maize anther. In a normal anther a hypodermal cell divides periclinally with the inner cell giving rise to the sporogenous archesporial cells while the outer cell, together with adjacent cells, forms the primary parietal layer. The cells of the parietal layer then undergo two cycles of periclinal divisions to give rise to three wall layers. In mac1 anthers the primary parietal layer usually fails to divide periclinally so that the three wall layers do not form, while the archesporial cells divide excessively and most fail to form microsporocytes. The centrally located mutant microsporocytes are abnormal in appearance and in callose distribution and they fail to proceed through meiosis. These failures in development and function appear to reflect the failure of mac1 gene function in the hypodermal cells and their cellular progeny.

The terminal differentiation factor LIN-29 is required for proper vulval morphogenesis and egg laying in Caenorhabditis elegans

Caenorhabditis elegans vulval development culminates during exit from the L4-to-adult molt with the formation of an opening through the adult hypodermis and cuticle that is used for egg laying and mating. Vulva formation requires the heterochronic gene lin-29, which triggers hypodermal cell terminal differentiation during the final molt. lin-29 mutants are unable to lay eggs or mate because no vulval opening forms; instead, a protrusion forms at the site of the vulva. We demonstrate through analysis of genetic mosaics that lin-29 is absolutely required in a small subset of lateral hypodermal seam cells, adjacent to the vulva, for wild-type vulva formation and egg laying. However, lin-29 function is not strictly limited to the lateral hypodermis. First, LIN-29 accumulates in many non-hypodermal cells with known roles in vulva formation or egg laying. Second, animals homozygous for one lin-29 allele, ga94, have the vulval defect and cannot lay eggs, despite having a terminally differentiated adult lateral hypodermis. Finally, vulval morphogenesis and egg laying requires lin-29 activity within the EMS lineage, a lineage that does not generate hypodermal cells.

A Screen for Genetic Loci Required for Hypodermal Cell and Glial-Like Cell Development During Caenorhabditis elegans Embryogenesis

The Caenorhabditis elegans lin-26 gene is expressed in all nonneuronal ectodermal cells. To identify genes required to specify the fates of ectodermal cells, we have conducted screens designed to identify loci whose zygotic function would be required for normal lin-26 expression. First, we examined 90 deficiencies covering 75% of the genome; second, we examined the progeny of 3600 genomes after EMS mutagenesis. We identified six loci that appear to be required for normal lin-26 expression. We argue that the deficiency eDf19 deletes a gene involved in specifying hypodermal cell fates. The genes emb-29 (previously known) and ale-1 (newly found) could be involved in a cell cycle function and/or in specifylng the fates of some precursors within different lineages that generate hypodermal cells and nonectodermal cells. We argue that the overlapping deficiencies qDf7, qDf8 and qDf9 delete a gene required to limit the number of nonneuronal ectodermal cells. We suggest that the deficiencies ozDf2, itDf2 and nDf42 delete genes required, directly or indirectly, to repress lin-26 expression in cells that normally do not express lin-26. We discuss the implications of these findings concerning the generation of the ectoderm.