Non-coding RNAs (ncRNAs) that were once considered “dark matter” or “transcriptional noise” in genomes are research hotspots in the field of epigenetics. The most well-known microRNAs (miRNAs) are a class of short non-coding, small molecular weight RNAs with lengths of 20–24 nucleotides that are highly conserved throughout evolution. Through complementary pairing with the bases of target sites, target gene transcripts are cleaved and degraded, or translation is inhibited, thus regulating the growth and development of organisms. Unlike miRNAs, which have been studied thoroughly, long non-coding RNAs (lncRNAs) are a group of poorly conserved RNA molecules with a sequence length of more than 200 nucleotides and no protein encoding capability; they interact with large molecules, such as DNA, RNA, and proteins, and regulate protein modification, chromatin remodeling, protein functional activity, and RNA metabolism in vivo through cis- or trans-activation at the transcriptional, post-transcriptional, and epigenetic levels. Research on plant lncRNAs is just beginning and has gradually emerged in the field of plant molecular biology. Currently, some studies have revealed that lncRNAs are extensively involved in plant growth and development and stress response processes by mediating the transmission and expression of genetic information. This paper systematically introduces lncRNA and its regulatory mechanisms, reviews the current status and progress of lncRNA research in plants, summarizes the main techniques and strategies of lncRNA research in recent years, and discusses existing problems and prospects, in order to provide ideas for further exploration and verification of the specific evolution of plant lncRNAs and their biological functions.

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SummaryDeep roots give rise to flourishing leaves, and the two complement each other. However, the genetic mechanisms underlying adventitious rooting for forest trees have remained elusive. In this study, we verified that peu‐miR160a targets six poplar genes AUXIN RESPONSE FACTORS (ARFs), PeARF10.1, PeARF16.1, PeARF16.2, PeARF16.3, PeARF17.1 and PeARF17.2, using 5’RLM‐RACE. Interaction experiments with peu‐miR160a and PeARFs in poplar protoplasts further confirmed that peu‐miR160a targets and negatively regulates the six PeARFs. Peu‐miR160a and its target genes exhibited obvious temporal expression in different stages of adventitious root development, and they could also be induced by IAA and abscisic acid. Peu‐miR160a‐overexpressing lines exhibited a significant shortening of adventitious root length, an increase in the number of lateral roots, severe dwarfing and shortened internodes. In addition, the overexpression of PeARF17.1 or mPeARF17.2 (peu‐miR160a‐resistant version of PeARF17.2) significantly increased the number of adventitious roots. Furthermore, PeARF17.1‐overexpressing lines had multiple branches with no visible trunk, although the adventitious root length of the PeARF17.1‐overexpressing lines was significantly increased. Our findings reveal that the peu‐miR160a − PeARF17.1/PeARF17.2 module is an important regulator involved in the development of the adventitious roots of poplar.

A population-based retrospective study was conducted in Harbin, China. The medical records of 13 711 singleton infants born between 2001 and 2005 in 16 hospitals were reviewed. The incidence of macrosomia (birthweight ‡4000 g) was found to have increased from 8.31% in 2001 to 10.50% in 2005. Over this period, the ponderal index decreased and birth length increased in infants with macrosomia. In a multivariate analysis, risk factors for delivery of a newborn with macrosomia were found to be high prepartal body mass index (BMI), maternal height ‡165 cm, male gender of the newborn, gestational age of 40-41.9 weeks, maternal age ‡30 years and a maternal diagnosis of hypertension. The increase in the incidence of macrosomia in Harbin was attributable to increases in maternal prepartal BMI, height and age in the population.

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The ability of a plant to form roots from its non-root tissues is ecologically advantageous during rapid adaptation to a changing environment. Although this biological phenomenon has been widely utilized for cuttings in many economically important agronomic and tree species, its genetic and developmental mechanisms have been poorly understood. In this study, we conducted an association analysis of small RNAs, the degradome and the transcriptome of adventitious rooting in poplar softwood cuttings, which revealed that 373 miRNA-target pairs were detected. Of these, 72 significantly differentially expressed targets were screened as likely to modulate adventitious root (AR) development, in conjunction with plant hormone signal transduction. Poplar miR167a and its targets PeARF6s and PeARF8s were subjected to functional verification of their ability to mediate plant growth and hormone signal transduction. Overexpression of miR167a inhibited target transcripts and improved lateral root (LR) development in poplar, while overexpressing PeARF8.1mut increased AR numbers and slightly inhibited LR development. Taken together, these results suggest that miR167a-PeARF8.1 modules play crucial roles in regulating AR and LR development in poplar and improve the adaptation of poplar to more complex environments.

Abstract.To elucidate the mechanisms of nuclear estrogen receptor (ER)-mediated and G protein-coupled receptor 30

Despite a number of studies on biomarkers in chronic obstructive pulmonary disease (COPD), only a few disease-related markers have been identified, yet we still have no satisfactory markers specific to innate immune system and neutrophil activation, which is essential in airway inflammation in COPD. Recent biological studies indicated that lipocalins (LCNs) might be involved in airway inflammation and innate immunity; however, results from available studies on the association of LCNs with COPD are not consistent. We carried out a multicenter prospective observational cohort study to investigate the differences in serum levels of LCN1 and LCN2 between subjects with COPD (n=58) and healthy controls (n=29). Several validated inflammatory markers, including C-reactive protein, tumor necrosis factor-α, interleukin-6, and interleukin-8, were measured. The correlation of LCN1 and LCN2 with clinical features such as smoking habits, lung function, symptoms, and disease category was also analyzed. When comparing with healthy controls, serum levels of LCN1 (66.35±20.26 ng/mL versus 41.16±24.19 ng/mL, P<0.001) and LCN2 (11.29±3.92 ng/mL versus 6.09±5.13 ng/mL, P<0.001) were both elevated in subjects with COPD after adjusting for age, sex, smoking habits, and inflammatory biomarkers. Smoking history and tobacco exposure, as quantified by pack-year, had no impact on systemic expressions of LCN1 and LCN2 in our study. Blood levels of LCN1 and LCN2, respectively, were negatively correlated to COPD Assessment Test and Modified Medical British Research Council score (P<0.001). Disease category by Global Initiative for Chronic Obstructive Lung Disease grade 1–4 or group A–D was not associated with levels of LCNs. Patient-reported exacerbations and body mass index were also tested, but no relationship with LCNs was found. In summary, serum concentrations of LCN1 and LCN2 were both elevated in patients with COPD, with their levels correlating to COPD Assessment Test and Modified Medical British Research Council score. These findings warrant large-scale and longitudinal studies to validate LCNs as circulating biomarkers for COPD.