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The thermophilic fungus Gymnascella thermotolerans GTE-21 produces a significant amount of both volatile and nonvolatile compounds with potent antifungal and anticancer properties. Gas chromatography-mass spectrometry (GC-MS) was utilized to identify 14 volatile organic compounds (VOCs) released by G. thermotolerans. The most predominant compound identified was diisooctyl phthalate, constituting 71.99% of the total VOCs, followed by phenol, 2-methoxy-4-(2-propenyl) at 7.12%. The GTE-21's VOCs demonstrated significant antifungal growth inhibition activity of 42.5% against Fusarium solani and 39.03% against Alternaria alternata. Additionally, GTE-21's crude extract exhibited substantial antibacterial effects, evidenced by inhibition zones of 1.5 cm against S. epidermidis, 1.4 cm against C. ciferrii, and 1.3 cm against S. aureus. The CHR2RClR2R:MeOH (1:1) fraction was more effective against human pathogens, producing the largest zones of inhibition of 1.1 and 1.03 cm against S. epidermidis and C. ciferrii, respectively. The evaluation of GTE-21's antifungal activity using the Evans blue assay showed that fungal spores treated with GTE-21's crude extract exhibited 96.2% inhibition at a concentration of 25 mg/ml. Similarly, the fractions CH2Cl2:MeOH (1:1) and CH2Cl2:MeOH (9:1) demonstrated spore inhibition rates of 96.3% and 94.3%, respectively. The EtOAc crude extract demonstrated pronounced cytotoxic effects against the SKOV-3 and MDA-MB-231 cancer cell lines. For SKOV-3, cell viability decreased to 3.40% and 0.47% at concentrations of 50 and 100 μL, respectively. In the case of MDA-MB-231, cell viability was reduced to 0.19% at both 50 and 100 μL concentrations. [ABSTRACT FROM AUTHOR]

The fruit rot disease of sweet melon is responsible for serious of economic crop losses that have occurred sporadically in Aswan, Egypt recently. The symptoms appeared as water-soaking lesion which advanced to the rotting of the fruit surface. White mycelial mats with brown color inside appear on the lesion at the surface of the fruit. Disease symptoms, morphological and mycological characteristics, pathogenicity and molecular identification, indicated as Fusarium solani, are the disease causative. When healthy fruits of sweet melon sprayed with spore suspension of the isolated F. solani, the disease symptoms appeared as white spot, which enlarged and turned brown. Dual culture techniques showed that the endophytic fungi, Aspergillus terreus, Fusarium solani and Penicillium verrucosum isolated from the medicinal plant Solenostemma arghel inhibited the pathogen growth in variable levels. The extract of ethyl acetate of the endophytic fungal was found to be active against Fusarium solani. The ethyl acetate fractions of Penicillium verrucosum inhibited the pathogen growth by 47% while A. terreus, and F. solani showed inhibition percentage of 45% and 40%, respectively [ABSTRACT FROM AUTHOR]

Plant microRNAs (miRNAs) associate with ARGONAUTE1 (AGO1) to direct post-transcriptional gene silencing and regulate numerous biological processes. Although AGO1 predominantly binds miRNAs in vivo, it also associates with endogenous small interfering RNAs (siRNAs). It is unclear whether the miRNA/siRNA balance affects miRNA activities. Here we report that FIERY1 (FRY1), which is involved in 5′−3′ RNA degradation, regulates miRNA abundance and function by suppressing the biogenesis of ribosomal RNA-derived siRNAs (risiRNAs). In mutants of FRY1 and the nuclear 5′−3′ exonuclease genes XRN2 and XRN3, we find that a large number of 21-nt risiRNAs are generated through an endogenous siRNA biogenesis pathway. The production of risiRNAs correlates with pre-rRNA processing defects in these mutants. We also show that these risiRNAs are loaded into AGO1, causing reduced loading of miRNAs. This study reveals a previously unknown link between rRNA processing and miRNA accumulation. Arabidopsis AGO1 binds both microRNA (miRNA) and endogenous small interfering RNA (siRNA). Here the authors show that 5′−3′ RNA degradation suppresses siRNA biogenesis from ribosomal RNA to prevent overloading of AGO1 with ribosomal siRNA and maintain miRNA-directed post translational gene silencing. [ABSTRACT FROM AUTHOR]