Biochemical recognition in seeds: Germination of Rumex obtusifolius is promoted by leaves of facilitative adult conspecifics

Seeds express various germination behaviors in response to competitor plants. However, germination behaviors in response to facilitator plants are not yet well understood. Rumex obtusifolius seedlings usually appear on the ground near adult conspecific plants, and their survival rate under the canopy of adult conspecifics is higher than that outside the canopy, indicating that adult R. obtusifolius plants facilitate their seedling establishments. We hypothesized that emergence of R. obtusifolius seedlings is promoted by cues from adult conspecifics, but emergence of heterospecific seedlings is not. To test this, we investigated emergence responses of seedlings of R. obtusifolius and three other species that grow with R. obtusifolius in the presence of R. obtusifolius leaf phytochemicals. Emergence of R. obtusifolius seedlings was promoted by the presence of R. obtusifolius leaves. In contrast, emergence of other species seedlings was not promoted by R. obtusifolius leaves. We conclude that germination of R. obtusifolius seeds is facilitated in the presence of conspecifics, via water-soluble chemical exposure, and that recognizing these chemicals has adaptive value.     

Structural Analysis of Free N-Glycans in α-Glucosidase Mutants of Saccharomyces cerevisiae: Lack of the Evidence for the Occurrence of Catabolic α-Glucosidase Acting on the N-Glycans

Saccharomyces cerevisiae produces two different α-glucosidases, Glucosidase 1 (Gls1) and Glucosidase 2 (Gls2), which are responsible for the removal of the glucose molecules from N-glycans (Glc₃Man₉GlcNAc₂) of glycoproteins in the endoplasmic reticulum. Whether any additional α-glucosidases playing a role in catabolizing the glucosylated N-glycans are produced by this yeast, however, remains unknown. We report herein on a search for additional α-glucosidases in S. cerevisiae. To this end, the precise structures of cytosolic free N-glycans (FNGs), mainly derived from the peptide:N-glycanase (Png1) mediated deglycosylation of N-glycoproteins were analyzed in the endoplasmic reticulum α-glucosidase-deficient mutants. 12 new glucosylated FNG structures were successfully identified through 2-dimentional HPLC analysis. On the other hand, non-glucosylated FNGs were not detected at all under any culture conditions. It can therefore be safely concluded that no catabolic α-glucosidases acting on N-glycans are produced by this yeast.     

Effect of twenty four wheat genotypes on soil biochemical and microbial properties

Plant and Soil - Understanding the effect of wheat genotype on soil properties will be crucial in breeding towards more sustainable wheat production and increased yield. We examined the...     

Towards the systematic discovery of signal transduction networks using phosphorylation dynamics data

Background  

Phosphorylation is a ubiquitous and fundamental regulatory mechanism that controls signal transduction in living cells. The number of identified phosphoproteins and their phosphosites is rapidly increasing as a result of recent mass spectrometry-based approaches.     

Quantitative analysis of the kinetics of phospholipase A2 using fast atom bombardment mass spectrometry

Fast atom bombardment mass spectrometry that can directly analyze lysophospholipids was used to quantitatively determine the kinetics of phospholipase A2. This method is 1250 times more sensitive than the colorimetric assay.     

miR-33a-5p in small extracellular vesicles as non-invasive biomarker for oxaliplatin sensitivity in human colorectal cancer cells

microRNAs (miRNAs) contained in small extracellular vesicles (sEVs) are candidates for non-invasive biomarkers. Oxaliplatin (L-OHP) has been approved for advanced colorectal cancer (CRC) chemotherapy. However, the response to L-OHP differs among CRC patients. In addition, CRC cells often acquire the resistance to L-OHP. This study aimed at the prediction of L-OHP sensitivity by measuring extracellular miRNAs levels. Firstly, we compared intracellular miRNAs expressions in L-OHP-sensitive CRC cells (SW620 and HCT116 cells) with those in acquired and intrinsic L-OHP-resistant cells. In microarray and real-time RT-PCR analyses, the intracellular miR-33a-5p, miR-210–3p, and miR-224–5p expressions were lower in acquired and intrinsic L-OHP-resistant CRC cells than sensitive cells. Furthermore, in SW620 cells, L-OHP sensitivity was decreased by miR-33a-5p inhibitor. On the other hand, miR-210–3p or miR-224–5p inhibitor did not affect L-OHP sensitivity in SW620 cells. Secondly, the amount of miR-33a-5p, miR-210–3p, and miR-224–5p in sEVs was compared. The amount of miR-33a-5p and miR-210–3p in sEVs secreted from acquired and intrinsic L-OHP-resistant cells tended to be small. miR-224–5p was not detected in sEVs secreted from three types of CRC cells examined. To the best of our knowledge, this is the first study demonstrating that miR-33a-5p and/or miR-210–3p in sEVs would be candidates for biomarkers of L-OHP sensitivity. In particular, miR-33a-5p is a promising candidate because it would be directly involved in L-OHP sensitivity.     

Photo-induced DNA cleavage reaction characteristics of propargylic sulfones possessing anthraquinone chromophore

DNA cleavage potency of propargylic sulfones possessing anthraquinone chromophore 1 under UV-irradiation was evaluated in comparison with the dark reaction. 1 showed inefficient DNA cleavage activity, while having considerably strong DNA binding ability. This result is accounted for by spatial conditions that the activated alkylating allenic site of intercalated 1 could not effectively approach to DNA bases, most probably guanine moiety, and thereby led to insufficient DNA strand cleavage. In contrast, the DNA cleavage activity of 1 was notably enhanced upon UV-irradiation (lambda(ex)=365 nm) followed by incubation. Under UV-irradiation, further DNA cleavage were occurred primary at 5'-G of GG steps within DNA. A DNA cleavage mechanism for 1, by which photo-induced one-electron oxidation of 5'-G of GG steps may occur along with ordinary alkylation, has been proposed.     

Aberrant RNA processing contributes to the pathogenesis of mitochondrial diseases in trans-mitochondrial mouse model carrying mitochondrial tRNALeu(UUR) with a pathogenic A2748G mutation

Mitochondrial tRNAs are indispensable for the intra-mitochondrial translation of genes related to respiratory subunits, and mutations in mitochondrial tRNA genes have been identified in various disease patients. However, the molecular mechanism underlying pathogenesis remains unclear due to the lack of animal models. Here, we established a mouse model, designated ‘mito-mice tRNA^Leu(UUR)2748’, that carries a pathogenic A2748G mutation in the tRNA^Leu(UUR) gene of mitochondrial DNA (mtDNA). The A2748G mutation is orthologous to the human A3302G mutation found in patients with mitochondrial diseases and diabetes. A2748G mtDNA was maternally inherited, equally distributed among tissues in individual mice, and its abundance did not change with age. At the molecular level, A2748G mutation is associated with aberrant processing of precursor mRNA containing tRNA^Leu(UUR) and mt-ND1, leading to a marked decrease in the steady-levels of ND1 protein and Complex I activity in tissues. Mito-mice tRNA^Leu(UUR)2748 with ≥50% A2748G mtDNA exhibited age-dependent metabolic defects including hyperglycemia, insulin insensitivity, and hepatic steatosis, resembling symptoms of patients carrying the A3302G mutation. This work demonstrates a valuable mouse model with an inheritable pathological A2748G mutation in mt-tRNA^Leu(UUR) that shows metabolic syndrome-like phenotypes at high heteroplasmy level. Furthermore, our findings provide molecular basis for understanding A3302G mutation-mediated mitochondrial disorders.