In flowering plants, RNA editing is a posttranscriptional mechanism that converts specific cytidines to uridines in both mitochondrial and plastidial transcripts, altering the information encoded by these genes. Here, we report the molecular characterization of the empty pericarp5 (emp5) mutants in maize (Zea mays). Null mutation of Emp5 results in abortion of embryo and endosperm development at early stages. Emp5 encodes a mitochondrion-targeted DYW subgroup pentatricopeptide repeat (PPR) protein. Analysis of the mitochondrial transcripts revealed that loss of the EMP5 function abolishes the C-to-U editing of ribosomal protein L16 at the rpl16-458 site (100% edited in the wild type), decreases the editing at nine sites in NADH dehydrogenase9 (nad9), cytochrome c oxidase3 (cox3), and ribosomal protein S12 (rps12), and surprisingly increases the editing at five sites of ATP synthase F0 subunit a (atp6), apocytochrome b (cob), nad1, and rpl16. Mutant EMP5-4 lacking the E+ and DYW domains still retains the substrate specificity and editing function, only at reduced efficiency. This suggests that the E+ and DYW domains of EMP5 are not essential to the EMP5 editing function but are necessary for efficiency. Analysis of the ortholog in rice (Oryza sativa) indicates that rice EMP5 has a conserved function in C-to-U editing of the rice mitochondrial rpl16-458 site. EMP5 knockdown expression in transgenics resulted in slow growth and defective seeds. These results demonstrate that Emp5 encodes a PPR-DYW protein that is required for the editing of multiple transcripts in mitochondria, and the editing events, particularly the Cto-U editing at the rpl16-458 site, are critical to the mitochondrial functions and, hence, to seed development in maize.

The aim of this study is to investigate cancer stem cells and their markers in the prostate cancer cell line Du145. Different populations of cells were isolated from Du145. The clones formed by CD44+ integrinalpha(2)beta(1)+CD133+ cells are remarkably different morphologically and quantitatively from those formed by integrinalpha(2)beta(1)(-/low)CD133(-) cells. CD133(+) cells have the capacity for self renewal, extensive differentiation potential, and high proliferative and tumorigenic potential. CD34+ and CD117+ cells have no stem cell properties. Expression levels of c-myc and beta-catenin were elevated and bax was down regulated in CD44+ integrinalpha(2)beta(1)+CD133+ cells. In summary, CD44, integrinalpha(2)beta(1) and CD133 could be the cancer stem cell makers for the Du145 cell line. CD133+ cells differed significantly from CD44+ integrinalpha(2)beta(1)(-/low)CD133- cells and the total population in clone generation, genes expression, differentiation, proliferative and tumorigenic potential.

In the field, close planting inevitably causes mutual shading and depression of leaf photosynthesis. To clarify the regulative mechanisms of photosynthesis under these conditions, the effects of planting density on leaf structure, gas exchange and proteomics were carefully studied in field-grown sorghum. In the absence of mineral deficiency, (1) close planting induced a significant decrease in light intensity within populations, which further resulted in much lower stomatal density and other anatomical characteristics associated with shaded leaves; (2) sorghum grown at high planting density had a lower net photosynthetic rate and stomatal conductance than those grown at low planting density; (3) approximately 62 protein spots changed their expression levels under the high planting density conditions, and 22 proteins associated with photosynthesis were identified by mass spectrometry. Further analysis revealed the depression of photosynthesis caused by mutual shading involves the regulation of leaf structure, absorption and transportation of CO2, photosynthetic electron transport, production of assimilatory power, and levels of enzymes related to the Calvin cycle. Additionally, heat shock protein and oxygen-evolving enhancer protein play important roles in photoprotection in field-grown sorghum. A model for the regulation of photosynthesis under mutual shading was suggested based on our results.

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