597. TULIPA SPRENGERI

Summary.  The distinctive Tulipa sprengeri Baker (Liliaceae) is illustrated and described. Its history, classification and cultivation requirements are discussed, including the results of recent research at Kew that establishes its position within the genus.     

598. TULIPA KOROLKOWII

Summary.  The Central Asian Tulipa korolkowii Regel is illustrated and described. Its history, classification, distribution and cultivation requirements are discussed.     

756. TULIPA UNDULATIFOLIA var. MICHELIANA

The new combination Tulipa undulatifolia var. micheliana is made and two Iranian forms are illustrated and described. The history and classification of this tulip are discussed and notes are provided on its distribution, natural habitat and cultivation requirements.     

miR-638 Regulates Differentiation and Proliferation in Leukemic Cells by Targeting Cyclin-dependent Kinase 2

MicroRNAs have been extensively studied as regulators of hematopoiesis and leukemogenesis. We identified miR-638 as a novel regulator in myeloid differentiation and proliferation of leukemic cells. We found that miR-638 was developmentally up-regulated in cells of myeloid but not lymphoid lineage. Furthermore, significant miR-638 down-regulation was observed in primary acute myeloid leukemia (AML) blasts, whereas miR-638 expression was dramatically up-regulated in primary AML blasts and leukemic cell lines undergoing forced myeloid differentiation. These observations suggest that miR-638 might play a role in myeloid differentiation, and its dysregulation may contribute to leukemogenesis. Indeed, ectopic expression of miR-638 promoted phorbol 12-myristate 13-acetate- or all-trans-retinoic acid-induced differentiation of leukemic cell lines and primary AML blasts, whereas miR-638 inhibition caused an opposite phenotype. Consistently, miR-638 overexpression induced G₁ cell cycle arrest and reduced colony formation in soft agar. Cyclin-dependent kinase 2 (CDK2) was found to be a target gene of miR-638. CDK2 inhibition phenotypically mimicked the overexpression of miR-638. Moreover, forced expression of CDK2 restored the proliferation and the colony-forming ability inhibited by miR-638. Our data suggest that miR-638 regulates proliferation and myeloid differentiation by targeting CDK2 and may serve as a novel target for leukemia therapy or marker for AML diagnosis and prognosis.     

Inoculation of hybrid poplar with the endophytic bacterium Enterobacter sp. 638 increases biomass but does not impact leaf level physiology

Endophytic bacteria have been shown to provide several advantages to their host, including enhanced growth. Inoculating biofuel species with endophytic bacteria is therefore an attractive option to increase the productivity of biofuel feedstocks. Here, we investigated the effect of inoculating hard wood cuttings of Populus deltoides Bartr. × Populus. nigra L. clone OP367 with Enterobacter sp. 638. After 17 weeks, plants inoculated with Enterobacter sp. 638 had 55% greater total biomass than un‐inoculated control plants. Study of gas exchange and fluorescence in developing and mature leaves over a diurnal cycle and over a 5 week measurement campaign revealed no effects of inoculation on photosynthesis, stomatal conductance, photosynthetic water use efficiency or the maximum and operating efficiency of photosystem II. However, plants inoculated with Enterobacter sp. 638 had a canopy that was 39% larger than control plants indicating that the enhanced growth was fueled by increased leaf area, not by improved physiology. Leaf nitrogen content was determined at two stages over the 5 week measurement period. No effect of Enterobacter sp. 638 on leaf nitrogen content was found indicating that the larger plants were acquiring sufficient nitrogen. Enterobacter sp. 638 lacks the genes for N₂ fixation, therefore the increased availability of nitrogen likely resulted from enhanced nitrogen acquisition by the 84% larger root system. These data show that Enterobacter sp. 638 has the potential to dramatically increase productivity in poplar. If fully realized in the production environment, these results indicate that an increase in the environmental and economic viability of poplar as a biofuel feedstock is possible when inoculated with endophytic bacteria like Enterobacter sp. 638.     

MicroRNA-638 inhibits cell proliferation by targeting phospholipase D1 in human gastric carcinoma

MicroRNAs (miRNAs) are a type of small non-coding RNAs that are often play important roles in carcinogenesis, but the carcinogenic mechanism of miRNAs is still unclear. This study will investigate the function and the mechanism of miR-638 in carcinoma (GC). The expression of miR-638 in GC and the DNA copy number of miR- 638 were detected by real-time PCR. The effect of miR-638 on cell proliferation was measured by counting kit-8 assay. Different assays, including bioinformatics algorithms (TargetScan and miRanda), luciferase report assay and Western blotting, were used to identify the target gene of miR-638 in GC. The expression of miR-638 target gene in clinical CRC tissues was also validated by immunohistochemical assay. From this research, we found that miR-638 was downregulated in GC tissues compared with corresponding noncancerous tissues (NCTs), and theDNAcopy numberof miR-638waslower in GC than NCTs, which may induce the corresponding downregulation of miR-638 in GC. Ectopic expression of miR-638 inhibited GC cell growth in vitro. Subsequently, we identified that PLD1 is the target gene of miR-638 in GC, and silencing PLD1 expression phenocopied the inhibitory effect of miR-638 on GC cell proliferation. Furthermore, we observed that PLD1 was overexpressed in GC tissues, and high expression of PLD1 in GC predicted poor overall survival. In summary, we revealed that miR- 638 functions as a tumor suppressor in GC through inhibiting PLD1.     

Downregulation of miR-638 promotes invasion and proliferation by regulating SOX2 and induces EMT in NSCLC

Aberrant expression of microRNAs has been shown to regulate the biological processes of lung cancer cells. However, the role of miR-638 in the development of NSCLC is still unclear. In this study, low miR-638 and high SOX2 were shown to be associated with tumor size and metastasis of NSCLC patients. Downregulated miR-638 could promote cell invasion and proliferation, while high miR-638 expression reversed the effect. Furthermore, miR-638 could regulate SOX2 by directly binding to its 3′-UTR. Silencing of SOX2 by siRNA partially abolished the enhancement of cell invasion and proliferation induced by downregulated miR-638. Aberrant miR-638 expression could modulate the expression levels of markers of epithelial-to-mesenchymal transition. Our results indicate that miR-638 may play a pivotal role in the development of NSCLC.