Exposure to adverse temperature conditions is a common stress factor for plants. In order to cope with heat stress, plants activate several defence mechanisms responsible for the control of reactive oxygen species (ROS) and redox homeostasis. Specific heat shocks (HSs) are also able to activate programmed cell death (PCD). In this paper, the alteration of several oxidative markers and ROS scavenging enzymes were studied after subjecting cells to two different HSs. Our results suggest that, under moderate HS, the redox homeostasis is mainly guaranteed by an increase in glutathione (GSH) content and in the ascorbate peroxidase (APX) and catalase (CAT) activities. These two enzymes undergo different regulatory mechanisms. On the other hand, the HS-induced PCD determines an increase in the activity of the enzymes recycling the ascorbate-and GSHoxidized forms and a reduction of APX; whereas, CAT decreases only after a transient rise of its activity, which occurs in spite of the decrease of its gene expression. These results suggest that the enzyme-dependent ROS scavenging is enhanced under moderate HS and suppressed under HS-induced PCD. Moreover, the APX suppression occurring very early during PCD, could represent a hallmark of cells that have activated a suicide programme.

Nitric oxide (NO) is a small redox molecule that acts as a signal in different physiological and stress-related processes in plants. Recent evidence suggests that the biological activity of NO is also mediated by S-nitrosylation, a well-known redox-based posttranslational protein modification. Here, we show that during programmed cell death (PCD), induced by both heat shock (HS) or hydrogen peroxide (H 2 O 2 ) in tobacco (Nicotiana tabacum) Bright Yellow-2 cells, an increase in S-nitrosylating agents occurred. NO increased in both experimentally induced PCDs, although with different intensities. In H 2 O 2 -treated cells, the increase in NO was lower than in cells exposed to HS. However, a simultaneous increase in S-nitrosoglutathione (GSNO), another NO source for S-nitrosylation, occurred in H 2 O 2 -treated cells, while a decrease in this metabolite was evident after HS. Consistently, different levels of activity and expression of GSNO reductase, the enzyme responsible for GSNO removal, were found in cells subjected to the two different PCD-inducing stimuli: low in H 2 O 2 -treated cells and high in the heat-shocked ones. Irrespective of the type of S-nitrosylating agent, S-nitrosylated proteins formed upon exposure to both of the PCD-inducing stimuli. Interestingly, cytosolic ascorbate peroxidase (cAPX), a key enzyme controlling H 2 O 2 levels in plants, was found to be S-nitrosylated at the onset of both PCDs. In vivo and in vitro experiments showed that S-nitrosylation of cAPX was responsible for the rapid decrease in its activity. The possibility that S-nitrosylation induces cAPX ubiquitination and degradation and acts as part of the signaling pathway leading to PCD is discussed.

We have studied InAs/GaSb superlattices (SLs) grown with either InSb-like or GaAs-like interfaces (IFs) on top of a GaSb buffer layer on (100) GaAs substrates. The InAs layer thickness was varied from 4 to 14 monolayers (ML) while the GaSb layer thickness was kept fixed at 10 ML. The type of IF bonds realized was verified by Raman scattering from mechanical IF modes. High-resolution X-ray diffraction using one- and two-dimensional mapping of symmetric and asymmetric reflections allowed us to determine independently the lattice parameters parallel and perpendicular to the growth direction. The GaSb buffer layer was found to be fully relaxed whereas the SLs with InSb-like IFs were coherently strained to the in-plane lattice parameter of the GaSb buffer for InAs layer thicknesses exceeding 6 ML. The strain distribution within the SLs with GaAs-like IFs was obtained from simulations of the X-ray reflection profiles. The SLs were found to be coherently strained close to the GaSb buffer and showed increasing strain relaxation with increasing distance from the buffer layer. In addition, these simulations provide an accurate determination of the SL periods. Well-resolved Raman spectra of backfolded longitudinal acoustic (LA) phonons were observed showing for SLs with ZnSb-like IFs folded LA phonon lines up to the seventh order. The spectrum of quasiconfined optical SL phonons was examined by Raman spectroscopy and by IR reflection. A detailed analysis of the IR reflection spectra allowed an independent determination of the individual layer widths within the SL stack, including the spatial extent of the GaAs-like IF mode

No abstract

Canine cutaneous mast cell tumour (CMCT) is a c-Kit driven tumour sharing similar c-Kit aberrations found in human gastrointestinal stromal tumour. CMCT is classified into three forms: well- (G1), intermediately (G2) (more benign diseases), and poorly (G3) differentiated (malignant) forms. We assess a correlation between c-Kit status, grading, and angiogenesis in CMCTs to explore their potential significance in humans. C-Kit receptor (c-KitR) expression, microvascular density (MVD), and mast cell granulated and degranulated status density (MCGD and MCDD, resp.) were analyzed in 97 CMCTs, by means of histochemistry, immunohistochemistry double staining, and image analysis system. Data showed that predominantly diffuse cytoplasmic- and predominantly focal paranuclear- (Golgi-like) c-Kit protein (PDC-c-Kit and PFP-c-Kit, resp.) expression correlate with high MVD, G3 histopathological grade, and MCDD. Moreover, predominant cell membrane-c-KitR (PCM-c-KitR) expression status correlates with low MVD, G1-G2 histopathological grade, and MCGD. These findings underline the key role of c-Kit in the biopathology of canine MCTs, indicating a link between aberrant c-Kit expression, increased angiogenesis, and higher histopathological grade. CMCT seems to be a model to study contributions of c-Kit activated MCs in tumour angiogenesis and to evaluate the inhibition of MCs activation by means of c-Kit tyrosine kinase inhibitors, currently translated in humans.