Induction of defence-related proteins by selected plant growth regulators and biocontrol agents against guava root knot nematode, Meloidogyne enterolobii.

Guava is an important edible and economic fruit crop distributed worldwide. It is widely infested with root knot nematode, Meloidogyne enterolobii which plays a vital role in causing economic losses. Several management strategies were performed to enhance the health status of guava and also to reduce root knot nematode infestation. Among the different aspects, application of plant growth regulators on guava plants under nursery conditions against root knot nematode, M. enterolobii was performed. The guava plants were treated with Salicylic acid (100 ppm), Jasmonic acid (100 ppm), and Indole 3-Butyric Acid (1000 ppm) alone and in combination of two and three. The result of this study revealed that IBA at 1,000 ppm alone (T3) and combined application of plant growth regulators viz., (T4) - Salicylic acid (100 ppm) + Jasmonic acid (100 ppm) + Indole 3-Butyric Acid (1,000 ppm) showed reduction in the nematode population and establishment of new roots (compensatory) and tertiary roots. The combined application of PGRs also increased the Plant height, root length, chlorophyll index, photosynthetic rate, transpiration rate, stomatal conductance, and chlorophyll fluorescence. The activity of various enzymes like total phenols, peroxidase, polyphenol oxidase, acid phosphatase, and phenylalanine ammonia lyase were influenced and developed resistance against root knot nematode, M. enterolobii. Under field conditions, application of Pochonia chlamydosporia and Purpureocilium lilacinum reduced the nematode infestation besides increasing the yield attributes of guava plants.

miR-24-2 regulates genes in survival pathway and demonstrates potential in reducing cellular viability in combination with docetaxel.

MicroRNAs the small (18-22 in length) noncoding RNA molecules are negative regulators of gene expression, modulating biological processes of cell differentiation, survival and death. The latter two phenomena are critical in tumour biology. We provide here the results of human genome wide target prediction of one such microRNA, hsa-miR-24-2, shown to target genes essential for initiating cellular stability and cell survival. The protein-protein interaction study showed important nodes which could affect cell cycle progression and differential oncogenesis. An analysis of hsa-miR-24-2 in sporadic breast tumours showed a negative correlation with metastasis and increasing nodes. The conclusion drawn of hsa-miR-24-2 targeting the genes of cell survival correlated with the methylation profile and resultant transcription factor binding site gain or loss in support of absence of cell survival. In order to accentuate the potential of hsa-miR-24-2 to reduce cellular viability under experimental conditions, in vitro studies in the presence and absence of anti-cancer drugs, such as docetaxel resulted in a significant decrease in cellular viability even at a 200-fold reduced dose of the drug in combination with hsa-miR-24-2.

MiR-101 induces senescence and prevents apoptosis in the background of DNA damage in MCF7 cells.

Moderately increased DNA damage due to the exogenous miR-101 (4 fold) over-expression in MCF7 cells was substantiated by an increase in the number of γ-H2AX foci, correlating with a simple-to-do Halo-assay. miR-101 induced mild/moderate DNA damage favoured senescence rather than apoptosis. An experimental support emanated from the induced mild/moderate DNA damage with 1 µM/5 µM etoposide in MCF7 cells, which resulted in an endogenous miR-101 over-expression (10/4 fold, respectively), followed by senescence. On the other hand, the severe DNA damage induced with 10 µM etoposide, resulted in a low (<1 fold) endogenous expression of miR-101 and an elevated percentage of apoptotic cells. Using bioinformatics tools along with in-vitro and in-vivo validations, miR-101 was found to target and downregulate the mRNA expression of UBE2N and SMARCA4, involved in DNA damage repair (DDR) pathways. Recovery of the expression of the two novel targets in anti-miR-101 transfection validated the results. We conclude that a threshold range of over-expressed miR-101, capable of inducing mild/moderate DNA damage, is sensed by cells to become senescent. The observation derives further support from in-silico protein-protein network analysis where the two novel targets showed their involvement in senescence pathway.

Solubilization of insoluble zinc compounds by Gluconacetobacter diazotrophicus and the detrimental action of zinc ion (Zn2+) and zinc chelates on root knot nematode Meloidogyne incognita.

AIM: To examine the zinc (Zn) solubilization potential and nematicidal properties of Gluconacetobacter diazotrophicus. METHODS AND RESULTS: Atomic Absorption Spectrophotometer, Differential Pulse Polarography and Gas Chromatography Coupled Mass Spectrometry were used to estimate the total Zn and Zn(2+) ions and identify the organic acids present in the culture supernatants. The effect of culture filtrate of Zn-amended G. diazotrophicus PAl5 on Meloidogyne incognita in tomato was examined under gnotobiotic conditions. Gluconacetobacter diazotrophicus PAl5 effectively solubilized the Zn compounds tested and 5-ketogluconic acid was identified as the major organic acid aiding the solubilization of zinc oxide. The presence of Zn compounds in the culture filtrates of G. diazotrophicus enhanced the mortality and reduced the root penetration of M. incognita under in vitro conditions. CONCLUSIONS: 5-ketogluconic acid produced by G. diazotrophicus mediated the solubilization process and the available Zn(2+) ions enhanced the nematicidal activity of G. diazotrophicus against M. incognita. SIGNIFICANCE AND IMPACT OF THE STUDY: Zn solubilization and enhanced nematicidal activity of Zn-amended G. diazotrophicus provides the possibility of exploiting it as a plant growth promoting bacteria.