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As with all aerial plant organs, fleshy fruits are encased in a hydrophobic cuticle that must fulfil multiple functions, including limiting desiccation and preventing microbial infection, which in the case of fruits maintains palatability and promotes seed dispersal. Fruit cuticles have many features in common with those of vegetative organs, but also have unique characteristics, including the fact that they are often astomatous, thicker than those of most leaves, and can be relatively easily isolated. These attributes provide a valuable experimental system to address questions related to cuticle structure, function, and the relationships between composition, architecture, permeability, and biomechanical properties. Here we provide an overview of insights into cuticle biology that have resulted from studies of those of fleshy fruits, as well as the diversity and dynamic nature of fruit cuticle composition and architecture, the environmental factors that influence those features, and the roles that they play in fruit ontogeny.

Senescent cells, formed in response to physiological and oncogenic stresses, facilitate protection from tumourigenesis and aid in tissue repair. However, accumulation of such cells in tissues contributes to age-related pathologies. Resistance of senescent cells to apoptotic stimuli may contribute to their accumulation, yet the molecular mechanisms allowing their prolonged viability are poorly characterized. Here we show that senescent cells upregulate the anti-apoptotic proteins BCL-W and BCL-XL. Joint inhibition of BCL-W and BCL-XL by siRNAs or the small-molecule ABT-737 specifically induces apoptosis in senescent cells. Notably, treatment of mice with ABT-737 efficiently eliminates senescent cells induced by DNA damage in the lungs as well as senescent cells formed in the epidermis by activation of p53 through transgenic p14 ARF . Elimination of senescent cells from the epidermis leads to an increase in hair-follicle stem cell proliferation. The finding that senescent cells can be eliminated pharmacologically paves the way to new strategies for the treatment of age-related pathologies. The accumulation of senescent cells within tissues plays a role in numerous age-related pathologies. Yosef and Pilpel et al . demonstrate that the resistance of these cells to apoptosis is driven by upregulation of survival proteins, whose pharmacological inhibition triggers senescent cell elimination in mice.

• Background and Aims The epidermis of an expanding dicot leaf is a mosaic of cells differing in identity, size and differentiation stage. Here hypotheses are tested that in such a cell mosaic growth is heterogeneous and changes with time, and that this heterogeneity is not dependent on the cell cycle regulation per se. • Methods Shape, size and growth of individual cells were followed with the aid of sequential replicas in expanding leaves of wild-type Arabidopsis thaliana and triple cyclinD3 mutant plants, and combined with ploidy estimation using epi-fluorescence microscopy. • Key Results Relative growth rates in area of individual epidermal cells or small cell groups differ several fold from those of adjacent cells, and change in time. This spatial and temporal variation is not related to the size of either the cell or the nucleus. Shape changes and growth within an individual cell are also heterogeneous: anticlinal wall waviness appears at different times in different wall portions; portions of the cell periphery in contact with different neighbours grow with different rates. This variation is not related to cell growth anisotropy. The heterogeneity is typical for both the wild type and cycD3. • Conclusions Growth of leaf epidermis exhibits spatiotemporal variability.

The surveillance of body barriers relies on resident T cells whose repertoires are biased toward particular γδ T cell antigen receptors (TCRs) according to location. These γδ TCRs can recognize ligands that emerge after stress. Through the use of intravital dynamics-immunosignal correlative microscopy, we found that γ-chain variable region 5 (V(γ)5) TCRs expressed by epidermal T cells were constitutively clustered and functionally activated in vivo at steady state, forming true immunological synapses that polarized and anchored T cell projections at squamous keratinocyte tight junctions. This synaptogenesis depended on TCR variable domains, the kinase Lck and the integrin α(E)[beta](7) but not the γδ lineage or the receptor NKG2D. In response to tissue stress, TCR-proximal signals did not increase substantially but underwent stress mode-dependent relocalization toward the basal epidermis and Langerhans cells. Thus, the γδ TCR orchestrates barrier surveillance proactively, presumably by recognizing tissue ligands expressed in the steady state.

The alternating cell specifications of root epidermis to form hair cells or nonhair cells in Arabidopsis are determined by the expression level of GL2, which is activated by an MYB–bHLH–WD40 (WER–GL3–TTG1) transcriptional complex. The phytohormone ethylene (ET) has a unique effect of inducing N-position epidermal cells to form root hairs. However, the molecular mechanisms underlying ET-induced ectopic root hair development remain enigmatic. Here, we show that ET promotes ectopic root hair formation through down-regulation of GL2 expression. ET-activated transcription factors EIN3 and its homolog EIL1 mediate this regulation. Molecular and biochemical analyses further revealed that EIN3 physically interacts with TTG1 and interferes with the interaction between TTG1 and GL3, resulting in reduced activation of GL2 by the WER–GL3–TTG1 complex. Furthermore, we found through genetic analysis that the master regulator of root hair elongation, RSL4, which is directly activated by EIN3, also participates in ET-induced ectopic root hair development. RSL4 negatively regulates the expression of GL2, likely through a mechanism similar to that of EIN3. Therefore, our work reveals that EIN3 may inhibit gene expression by affecting the formation of transcription-activating protein complexes and suggests an unexpected mutual inhibition between the hair elongation factor, RSL4, and the hair specification factor, GL2. Overall, this study provides a molecular framework for the integration of ET signaling and intrinsic root hair development pathway in modulating root epidermal cell specification.

The incidence of hypertension and cardiovascular disease (CVD) correlates with latitude and rises in winter. The molecular basis for this remains obscure. As nitric oxide (NO) metabolites are abundant in human skin, we hypothesized that exposure to UVA may mobilize NO bioactivity into the circulation to exert beneficial cardiovascular effects independently of vitamin D. In 24 healthy volunteers, irradiation of the skin with two standard erythemal doses of UVA lowered blood pressure (BP), with concomitant decreases in circulating nitrate and rises in nitrite concentrations. Unexpectedly, acute dietary intervention aimed at modulating systemic nitrate availability had no effect on UV-induced hemodynamic changes, indicating that cardiovascular effects were not mediated via direct utilization of circulating nitrate. UVA irradiation of the forearm caused increased blood flow independently of NO synthase (NOS) activity, suggesting involvement of pre-formed cutaneous NO stores. Confocal fluorescence microscopy studies of human skin pre-labeled with the NO-imaging probe diaminofluorescein 2 diacetate revealed that UVA-induced NO release occurs in a NOS-independent, dose-dependent manner, with the majority of the light-sensitive NO pool in the upper epidermis. Collectively, our data provide mechanistic insights into an important function of the skin in modulating systemic NO bioavailability, which may account for the latitudinal and seasonal variations of BP and CVD.

The surveillance of body barriers relies on resident T cells whose repertoires are biased toward particular γδ T cell antigen receptors (TCRs) according to location. These γδ TCRs can recognize ligands that emerge after stress. Through the use of intravital dynamics-immunosignal correlative microscopy, we found that γ-chain variable region 5 (Vγ 5) TCRs expressed by epidermal T cells were constitutively clustered and functionally activated in vivo at steady state, forming true immunological synapses that polarized and anchored T cell projections at squamous keratinocyte tight junctions. This synaptogenesis depended on TCR variable domains, the kinase Lck and the integrin αE β7 but not the γδ lineage or the receptor NKG2D. In response to tissue stress, TCR-proximal signals did not increase substantially but underwent stress mode-dependent relocalization toward the basal epidermis and Langerhans cells. Thus, the γδ TCR orchestrates barrier surveillance proactively, presumably by recognizing tissue ligands expressed in the steady state.

Successful fertilization relies on the production and effective release of viable pollen. Failure of anther opening (dehiscence), results in male sterility, although the pollen may be fully functional. MYB26 regulates the formation of secondary thickening in the anther endothecium, which is critical for anther dehiscence and fertility. Here, we show that although the MYB26 transcript shows expression in multiple floral organs, the MYB26 protein is localized specifically to the anther endothecium nuclei and that it directly regulates two NAC domain genes, NST1 and NST2, which are critical for the induction of secondary thickening biosynthesis genes. However, there is a complex relationship of regulation between these genes and MYB26. Using DEX-inducible MYB26 lines and overexpression in the various mutant backgrounds, we have shown that MYB26 up-regulates both NST1 and NST2 expression. Surprisingly normal thickening and fertility rescue does not occur in the absence of MYB26, even with constitutively induced NST1 and NST2, suggesting an additional essential role for MYB26 in this regulation. Combined overexpression of NST1 and NST2 in myb26 facilitates limited ectopic thickening in the anther epidermis, but not in the endothecium, and thus fails to rescue dehiscence. Therefore, by a series of regulatory controls through MYB26, NST1, NST2, secondary thickening is formed specifically within the endothecium; this specificity is essential for anther opening.