Differences in gene modulation in Saccharomyces cerevisiae indicate that maturity plays an important role in the high hydrostatic pressure stress response and resistance.

There is a strong relationship between the regulatory pathways to oxidative stress, longevity, and aging. High hydrostatic pressure (HHP) induces oxidative stress and activates cellular defense mechanisms. The understanding of these mechanisms is a strategy to delay damage associated with aging. Addressing resistance to stress and aging in Saccharomyces cerevisiae is a well-accepted approach since pathways involved in energy balance, damage accumulation and stress response are preserved among eukaryotes. The purpose of this study was to correlate the environmental stress response to cell maturity. HHP stress response on S. cerevisiae mother and daughter cells was evaluated through survival, reactive oxygen species (ROS) accumulation and gene expression. Mature cells were yeasts that had budded and originated at least one descendant, and young cells were the ones that did not form a bud. Mature cells were more resistant to HHP, although they showed a decrease in expression of antioxidants enzymes genes, and a higher intracellular levels of ROS. Young cells had less resistance to HHP despite a tendency of positively regulating these same antioxidant encoders. The TOR1 gene, related to aging and apoptosis, was unchanged in mother cells and showed a tendency toward increased expression in daughter cells submitted to HHP. The gene modulation differences of the mother and daughter cells indicates that maturity plays an important role in the HHP stress response and resistance. Thus, even accumulating high levels of ROS, mature cells were more tolerant to HHP stress and survived better, despite aging.

Transcriptome analysis provides insights into the delayed sticky disease symptoms in Carica papaya.

KEY MESSAGE: Global gene expression analysis indicates host stress responses, mainly those mediated by SA, associated to the tolerance to sticky disease symptoms at pre-flowering stage in Carica papaya. Carica papaya plants develop the papaya sticky disease (PSD) as a result of the combined infection of papaya meleira virus (PMeV) and papaya meleira virus 2 (PMeV2), or PMeV complex. PSD symptoms appear only after C. papaya flowers. To understand the mechanisms involved in this phenomenon, the global gene expression patterns of PMeV complex-infected C. papaya at pre-and post-flowering stages were assessed by RNA-Seq. The result was 633 and 88 differentially expressed genes at pre- and post-flowering stages, respectively. At pre-flowering stage, genes related to stress and transport were up-regulated while metabolism-related genes were down-regulated. It was observed that induction of several salicylic acid (SA)-activated genes, including PR1, PR2, PR5, WRKY transcription factors, ROS and callose genes, suggesting SA signaling involvement in the delayed symptoms. In fact, pre-flowering C. papaya treated with exogenous SA showed a tendency to decrease the PMeV and PMeV2 loads when compared to control plants. However, pre-flowering C. papaya also accumulated transcripts encoding a NPR1-inhibitor (NPR1-I/NIM1-I) candidate, genes coding for UDP-glucosyltransferases (UGTs) and several genes involved with ethylene pathway, known to be negative regulators of SA signaling. At post-flowering, when PSD symptoms appeared, the down-regulation of PR-1 encoding gene and the induction of BSMT1 and JA metabolism-related genes were observed. Hence, SA signaling likely operates at the pre-flowering stage of PMeV complex-infected C. papaya inhibiting the development of PSD symptoms, but the induction of its negative regulators prevents the full-scale and long-lasting tolerance.

A current overview of the Papaya meleira virus, an unusual plant virus.

Papaya meleira virus (PMeV) is the causal agent of papaya sticky disease, which is characterized by a spontaneous exudation of fluid and aqueous latex from the papaya fruit and leaves. The latex oxidizes after atmospheric exposure, resulting in a sticky feature on the fruit from which the name of the disease originates. PMeV is an isometric virus particle with a double-stranded RNA (dsRNA) genome of approximately 12 Kb. Unusual for a plant virus, PMeV particles are localized on and linked to the polymers present in the latex. The ability of the PMeV to inhabit such a hostile environment demonstrates an intriguing interaction of the virus with the papaya. A hypersensitivity response is triggered against PMeV infection, and there is a reduction in the proteolytic activity of papaya latex during sticky disease. In papaya leaf tissues, stress responsive proteins, mostly calreticulin and proteasome-related proteins, are up regulated and proteins related to metabolism are down-regulated. Additionally, PMeV modifies the transcription of several miRNAs involved in the modulation of genes related to the ubiquitin-proteasome system. Until now, no PMeV resistant papaya genotype has been identified and roguing is the only viral control strategy available. However, a single inoculation of papaya plants with PMeV dsRNA delayed the progress of viral infection.

Comparative analysis of the genomes of two isolates of cowpea aphid-borne mosaic virus (CABMV) obtained from different hosts.

The complete genomic sequences of two cowpea aphid-borne mosaic virus (CABMV) isolates from Brazil, MG-Avr from passion fruit (which also infects cowpea), and BR1 from peanut (which also infects cowpea, but not passion fruit), were determined. Their nucleotide sequences are 89% identical and display 85% identity to that of CABMV-Z. Both isolates have the typical potyvirus genome features. P3 and VPg are the most conserved proteins, with 99% amino acid sequence identity between the two isolates, and P1 is the most variable, with 50% identity. A significant variation exists at the 5'-end of the genome between the Brazilian isolates and CABMV-Z. However, this variation does not correlate with the biological properties of these three isolates.