Introduction: Wheat (Triticum aestivum L.) is among the world's most important staple food crops. In the current climate change scenario, a better understanding of wheat response mechanisms to water stress could help to enhance its productivity in arid ecosystems. Methods: In this study, water relations, gas exchange, membrane integrity, agronomic traits and molecular analysis were evaluated in six wheat genotypes (D117, Syndiouk, Tunisian durum7 (Td7), Utique, Mahmoudi AG3 and BT) subjected to drought-stress. Results and discussion: For all the studied genotypes, drought stress altered leaf area, chlorophyll content, stomatal density, photosynthetic rate and water-use efficiency, while the relative water content at turgor loss point (RWC0) remained stable. Changes in osmotic potential at turgor loss point (??0), bulk modulus of elasticity (?max) and stomatal regulation, differed greatly among the studied genotypes. For the drought-sensitive genotypes AG3 and BT, no significant changes were observed in ??0, whereas the stomatal conductance (gs) and transpiration rate (E) decreased under stress conditions. These two varieties avoided turgor loss during drought treatment through an accurate stomatal control, resulting in a significant reduction in yield components. On the contrary, for Syndiouk, D117, Td7 and Utique genotypes, a solute accumulation and an increase in cell wall rigidity were the main mechanisms developed during drought stress. These mechanisms were efficient in enhancing soil water uptake, limiting leaf water loss and protecting cells membranes against leakage induced by oxidative damages. Furthermore, leaf soluble sugars accumulation was the major component of osmotic adjustment in drought-stressed wheat plants. The transcriptional analysis of genes involved in the final step of the ABA biosynthesis (AAO) and in the synthesis of an aquaporin (PIP2:1) revealed distinct responses to drought stress among the selected genotypes. In the resistant genotypes, PIP2:1 was significantly upregulated whereas in the sensitive ones, its expression showed only a slight induction. Conversely, the sensitive genotypes exhibited higher levels of AAO gene expression compared to the resistant genotypes. Our results suggest that drought tolerance in wheat is regulated by the interaction between the dynamics of leaf water status and stomatal behavior. Based on our findings, Syndiouk, D117, Utique and Td7, could be used in breeding programs for developing high-yielding and drought-tolerant wheat varieties.

Transcriptional regulation is fundamental to most biological processes and reverse-engineering programs can be used to decipher the underlying programs. In this review, we describe how genomics is offering a systems biology-based perspective of the intricate and temporally coordinated transcriptional programs that control neuronal apoptosis and survival. In addition to providing a new standpoint in human pathology focused on the regulatory program, cracking the code of neuronal cell fate may offer innovative therapeutic approaches focused on downstream targets and regulatory networks. Similar to computers, where faults often arise from a software bug, neuronal fate may critically depend on its transcription program. Thus, cracking the code of neuronal life or death may help finding a patch for neurodegeneration and cancer.

Ochratoxin A (OTA) is a nephrotoxic and potentially carcinogenic mycotoxin produced by several species of Aspergillus and Penicillium, contaminating grapes, wine and a variety of food products. We recently isolated from soil a novel free-living Acinetobacter strain, named Acinetobacter sp. neg1, able to degrade OTA. Biochemical studies demonstrated that Acinetobacter sp. neg1 was able to degrade OTA into the not toxic catabolic product OTalpha (OT?), suggesting that the degradation reaction proceeds via peptide bond hydrolysis with phenylalanine release. The identification of the enzymes and biochemical pathway responsible for the degradation is the first step in the development of biotechnology applications for OTA reduction in the food chain. In order to find genes responsible for OTA degradation we made a differential expression analysis of Acinetobacter sp. neg1 grown in the presence or absence of the toxin. Briefly, total RNA was isolated from bacteria grown in the two conditions and mRNA was selectively enriched through rRNA depletion. Samples were then fragmented and used to obtain cDNA libraries that were sequenced with the Illumina MiSeq system, obtaining 4 x 106 paired-end reads. Reads were aligned to the reference genome using GSNAP software. Then, Cuffdiff was used to detect significant differences between the two conditions. This analysis revealed more than 100 differential expressed genes. Among them, 6 genes code for peptidases and resulted up-regulated at 6 hours. The enrichment analysis for Gene Ontology terms by the Java-based tool Bingo (included as a plugin in Cytoscape) revealed the over-representation of pathways which could be involved or consequent to OTA degradation, such as peptidase activity and protein and amino acid metabolic process and transport. These results confirmed that OTA degradation proceeds through peptidase activities. Furthermore, some molecular functions related to phenylalanine catabolism resulted dysregulated, suggesting that phenylalanine is an energy source for Acinetobacter sp. neg1 and the OTA degrading reaction is followed by the modulation of further catabolic activities.

Ochratoxin A (OTA) is a nephrotoxic and potentially carcinogenic mycotoxin produced by several species of Aspergillus and Penicillium, contaminating grapes, wine and a variety of food products. We recently isolated from soil a novel free-living Acinetobacter strain, named Acinetobacter sp. neg1, able to degrade OTA. Biochemical studies demonstrated that Acinetobacter sp. neg1 was able to degrade OTA into the not toxic catabolic product OTalpha (OT?), suggesting that the degradation reaction proceeds via peptide bond hydrolysis with phenylalanine release. The identification of the enzymes and biochemical pathway responsible for the degradation is the first step in the development of biotechnology applications for OTA reduction in the food chain. Numerous potential peptidase encoding genes are present in the genome of Acinetobacter sp. neg1, but in the absence of a comprehensive evaluation of the capacity of members of the genus to degrade OTA, the identification of candidate genes through comparative genomic approaches remains difficult. In order to find genes responsible for OTA degradation we made a differential expression analysis of Acinetobacter sp. neg1 grown in the presence or absence of the toxin. Briefly, total RNA was isolated from bacteria grown in the two conditions and mRNA was selectively enriched through rRNA depletion. Samples were then fragmented and used to obtain cDNA libraries that were sequenced with the Illumina MiSeq system, obtaining 4 x 106 paired-end reads with an average per base quality score > 30. The RNA seq data were analyzed in the discovery environment of iplant (http://www.iplantcollaborative.org/). In particular, reads were aligned to the reference genome using TopHat2. Then, Cuffdiff was used to calculate RPKM and detect significant differences between the two conditions. This analysis revealed more than 100 differential expressed genes. Among them, we found 4 genes coding for peptidases or hydrolases that could be involved in the reaction of degradation: 2 serine-type endopeptidases were up-regulated at 6 hours, while one aminopeptidase and one hydrolase were up-regolated at 12 hours. The enrichment analysis for Gene Ontology terms revealed the over-representation of molecular functions which could be involved or consequent to OTA degradation, such as serine-type endopeptidase activity, amino acid transmembrane transporter activity, D-amino acid metabolic process and protein maturation. These results confirmed that OTA degradation proceeds through peptidase activities. We hypothesize that this reaction induces the activation of pathways potentially involved in the phenylalanine metabolism. Further analysis are ongoing to verify the OTA degradation activity of the candidate genes.

To highlight different transcriptional behaviors of the phytoplasma in the plant and animal host, expression of 14 genes of "Candidatus Phytoplasma asteris," chrysanthemum yellows strain, was investigated at different times following the infection of a plant host (Arabidopsis thaliana) and two insect vector species (Macrosteles quadripunctulatus and Euscelidius variegatus). Target genes were selected among those encoding antigenic membrane proteins, membrane transporters, secreted proteins, and general enzymes. Transcripts were detected for all analyzed genes in the three hosts; in particular, those encoding the antigenic membrane protein Amp, elements of the mechanosensitive channel, and two of the four secreted proteins (SAP54 and TENGU) were highly accumulated, suggesting that they play important roles in phytoplasma physiology during the infection cycle. Most transcripts were present at higher abundance in the plant host than in the insect hosts. Generally, transcript levels of the selected genes decreased significantly during infection of A. thaliana and M. quadripunctulatus but were more constant in E. variegatus. Such decreases may be explained by the fact that only a fraction of the phytoplasma population was transcribing, while the remaining part was aging to a stationary phase. This strategy might improve long-term survival, thereby increasing the likelihood that the pathogen may be acquired by a vector and/or inoculated to a healthy plant.

The FAR1 gene encodes an 830 residue bifunctional protein, whose major function is inhibition of cyclindependent kinase complexes involved in the G1/S transition. FAR1 transcription is maximal between mitosis and early G1 phase. Enhanced FAR1 transcription is necessary but not sufficient for the pheromone-induced G1 arrest, since FAR1 overexpression itself does not trigger cell cycle arrest. Besides its well established role in the response to pheromone, recent evidences suggest that Far1 may also regulate the mitotic cell cycle progression: in particular, it has been proposed that Far1, together with the G1 cyclin Cln3, may be part of a cell sizer mechanismthat controls the entry into S phase. Far1 is an unstable protein throughout the cell cycle except during G1 phase. Far1 levels peak in newborn cells as a consequence of a burst of synthetic activity at the end of the previous cycle, and the amounts per cell remain roughly constant during the G1 phase. Phosphorylation (at serine 87) by Cdk1-Cln complexes primes Far1 for ubiquitin-mediated proteolysis. By coupling a genome-wide transcriptional analysis of FAR1-overexpressing and far1? cells grown in ethanolor glucose-supplemented minimal media with a range of phenotypic analysis, we show that FAR1 overexpression not only coordinately increases RNA and protein accumulation, but induces strong transcriptional remodeling, metabolism being the most affected cellular property, suggesting that the Far1/Cln3 sizer regulates cell growth either directly or indirectly by affecting metabolism and pathways known to modulate ribosome biogenesis. A crucial role in mediating the effect of Far1 overexpression is played by the Sfp1 protein, a key transcriptional regulator of ribosome biogenesis, whose presence ismandatory to allowa coordinated increase in both RNA and protein levels in ethanol-grown cells.