As one of the major groups of small post-translationally modified peptides, the CLV3/EMBRYO SURROUNDING REGION-RELATED (CLE)-like (CLEL) peptide family has been reported to regulate root growth, lateral root development and plant gravitropic responses in Arabidopsis thaliana. In this study, we identified 12 CLEL genes in Populus trichocarpa and performed a comprehensive bioinformatics analysis on these genes. Among them, five P. trichocarpa CLELs (PtrCLELs) were revised with new gene models. All of these PtrCLEL proteins were structurally similar to the A. thaliana CLELs (AtCLELs), including an N-terminal signal peptide, a conserved C-terminal 13-amino-acid CLEL motif and a variable intermediate region. In silico and quantitative real-time PCR analyses showed that PtrCLELs were widely expressed in various tissues, including roots, leaves, buds and stems. Exogenous application of chemically synthesized PtrCLEL peptides resulted in wavy or curly roots and reduced lateral root formation in A. thaliana. Moreover, germinating Populus deltoides seedlings on a growth medium containing these peptides caused the roots to thicken and to form abnormal lateral roots, in many cases in clusters. Anatomical and histological changes in thickened roots were further investigated by treating Populus 717 cuttings with the PtrCLEL10 peptide. We observed that root thickening was mainly due to an increased number of cells in the epidermis, hypodermis and cortex. The results of our study suggested that PtrCLEL and AtCLEL genes encode proteins with similar protein structures, sequences of peptide motif and peptide activities on developing roots. The activities of PtrCLEL peptides in root development were species-dependent.

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China’s government launched a policy in October 2017 to permit the distributed generators to peer-to-peer trade their electricity generation on the market. Several clauses in the policy document are, however, unclear and ambiguous. This work identifies three vital but not clearly detailed issues in the policy document: (1) participation eligibility, (2) the grid fee calculation method, and (3) subsidy rates. Then, we carry out a comprehensive analysis of the economic impacts of the trade policy based on a case study of an eastern city in China. Sensitivity analyses on the impacts of the subsidy rates, transmission and distribution prices (TDPs), and end-user regulated prices are conducted. The results show that the trading policy will benefit the photovoltaic (PV) generators with more revenue by 6–11%, reduce the cost for end-users by 6–12%, and decrease the revenue of the power grid company by 32–55%.

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Neuroblastoma is an important problem in children. Long noncoding RNAs (lncRNAs) exhibit important roles in tumorigenicity of neuroblastoma. However, the role and mechanism of lncRNA small nucleolar RNA host gene 16 (SNHG16) in neuroblastoma tumorigenicity remain poorly understood. Forty-six neuroblastoma samples and 28 normal tissues were harvested. The levels of SNHG16, microRNA-15b-5p (miR-15b-5p), and phosphoribosyl pyrophosphate synthetase 1 (PRPS1) were detected via quantitative reverse transcription PCR or western blot. Cell proliferation as well as cycle distribution were measured via 3-(4, 5-Dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide or flow cytometry. Cell metastasis was investigated via epithelial–mesenchymal transition or transwell assay. The target relationship of miR-15b-5p and SNHG16 or PRPS1 was explored via starBase and dual-luciferase reporter assay. The role of SNHG16 in neuroblastoma in vivo was analyzed using a xenograft model. We found SNHG16 and PRPS1 levels were increased in neuroblastoma tissues and cells. SNHG16 knockdown inhibited cell proliferation, increased the cell cycle distribution at G0/G1 phase, and decreased the cells at S phase. SNHG16 overexpression caused an opposite effect. SNHG16 silence suppressed neuroblastoma cell metastasis. PRPS1 knockdown constrained cell proliferation and metastasis and regulated cell cycle distribution. miR-15b-5p was sponged by SNHG16 and directly targeted PRPS1. miR-15b-5p knockdown or PRPS1 overexpression mitigated the influence of SNHG16 silence on cell cycle, proliferation, and metastasis. SNHG16 knockdown reduced xenograft tumor growth. In conclusion, SNHG16 downregulation suppressed neuroblastoma tumorigenicity by regulating cell cycle, proliferation, and metastasis via miR-15b-5p/PRPS1 axis.