Fluorescent Pseudomonas (FP) is a major group of plant growth promoting rhizobacteria and a well-known synthesizer of siderophores, which imparts a selective advantage on rhizosphere competence and their biocontrol traits. The present study was aimed at examining the factors affecting the production of siderophores and their potential biocontrol traits. Sixteen FP isolates were shortlisted based on their siderophore-producing ability in chrome azural S medium. The isolates were checked for variations in siderophore production under varying incubation times, temperatures, pH, iron (Fe3+) concentrations and mutagens. In addition, the iron binding affinity of siderophores, mycelial inhibition assay and plant growth promotion traits were assessed. Results showed that the siderophore production was highly influenced by the time of incubation, changes in pH, temperature and iron concentration. Chemical characterization showed that the produced siderophores were hydroxamates. Maximum siderophore production was observed at pH 7 whereas UV and EtBr exposure invariably suppressed siderophore production drastically in all isolates. All FPs from maize rhizosphere showed excellent siderophore production which could be due to the competence in strategy-II of the plant rhizosphere and significant growth inhibition on Fusarium oxysporum. Our results suggest the inclination of siderophores to iron, in terms of various criteria affecting production and the possible role of environmental mutations that affect the natural iron harvesting mechanism.

Suberoylanilide hydroxamic acid (SAHA) is a histone deacetylase inhibitor (HDACi) that suppresses the growth of tumor cells in humans and canines. SAHA reportedly enhances the antitumor activity of human peripheral blood mononuclear cell (PBMC). However, it is unclear whether a similar effect is exerted in canines. The present study focused on the effect of SAHA on the cytotoxicity of IL-2 activated PBMC in three tumor cell lines (CTAC, CIPm, and MCM-N1). The mRNA expression of a ligand for the NKG2D receptor was upregulated in SAHA-treated cell lines. Moreover, the SAHA-treated cell lines, except MCM-N1 demonstrated a significantly higher PBMC cytotoxicity compared to the untreated cell lines. Therefore, the NKG2DL upregulation likely enhanced the interaction of NKG2D-NKG2DL, leading to enhanced cytotoxicity of PBMC. It was also revealed that activated PBMC treated with SAHA significantly attenuated their cytotoxicity toward all the cell lines. Although the NKG2D, NKp46, NKp44, and NKp30 receptors, involved in PBMC cytotoxicity, were presumed to be downregulated, there was no significant reduction in the mRNA expression of these receptors. This study revealed that SAHA not only sensitizes the canine tumor cells to cytotoxicity due to PBMC activation, but also suppresses the cytotoxicity of PBMC themselves. Therefore, our results highlight the necessity of avoiding this inhibitory action to enhance the antitumor effect of SAHA in canines.