Grain size determines grain weight and affects grain quality. Several major quantitative trait loci (QTLs) regulating grain size have been cloned; however, our understanding of the underlying mechanism that regulates the size of rice grains remains fragmentary. Here, we report the cloning and characterization of a dominant QTL, grain size on chromosome 2 (GS2), which encodes Growth-Regulating Factor 4 (OsGRF4), a transcriptional regulator. GS2 localizes to the nucleus and may act as a transcription activator. A rare mutation of GS2 affecting the binding site of a microRNA, OsmiR396c, causes elevated expression of GS2/OsGRF4. The increase in GS2 expression leads to larger cells and increased numbers of cells, which thus enhances grain weight and yield. The introduction of this rare allele of GS2/OsGRF4 into rice cultivars could significantly enhance grain weight and increase grain yield, with possible applications in breeding high-yield rice varieties.

BackgroundGestational diabetes mellitus (GDM) is one type of diabetes that presents during pregnancy and significantly increases the risk of a number of adverse consequences for the fetus and mother. The microRNAs (miRNA) have recently been demonstrated to abundantly and stably exist in serum and to be potentially disease-specific. However, no reported study investigates the associations between serum miRNA and GDM.Methodology/Principal FindingsWe systematically used the TaqMan Low Density Array followed by individual quantitative reverse transcription polymerase chain reaction assays to screen miRNAs in serum collected at 16–19 gestational weeks. The expression levels of three miRNAs (miR-132, miR-29a and miR-222) were significantly decreased in GDM women with respect to the controls in similar gestational weeks in our discovery evaluation and internal validation, and two miRNAs (miR-29a and miR-222) were also consistently validated in two-centric external validation sample sets. In addition, the knockdown of miR-29a could increase Insulin-induced gene 1 (Insig1) expression level and subsequently the level of Phosphoenolpyruvate Carboxy Kinase2 (PCK2) in HepG2 cell lines.Conclusions/SignificanceSerum miRNAs are differentially expressed between GDM women and controls and could be candidate biomarkers for predicting GDM. The utility of miR-29a, miR-222 and miR-132 as serum-based non-invasive biomarkers warrants further evaluation and optimization.

Omental adipose tissue plays a central role in insulin resistance in gestational diabetes mellitus (GDM), and the molecular mechanisms leading to GDM remains vague. Evidence demonstrates that maternal hormones, such as estradiol, contribute to insulin resistance in GDM. In this study we determined the differential expression patterns of microRNAs (miRNAs) in omental adipose tissues from GDM patients and pregnant women with normal glucose tolerance using AFFX miRNA expression chips. MiR-222, 1 of 17 identified differentially expressed miRNAs, was found to be significantly up-regulated in GDM by quantitative real-time PCR (P < .01), and its expression was closely related with serum estradiol level (P < .05). Furthermore, miR-222 expression was significantly increased in 3T3-L1 adipocytes with a high concentration of 17β-estradiol stimulation (P < .01), whereas the expressions of estrogen receptor (ER)-α protein and insulin-sensitive membrane transporter glucose transporter 4 (GLUT4) protein (P < .01) were markedly reduced. In addition, ERα was shown to be a direct target of miR-222 in 3T3-L1 adipocytes by using the luciferase assay. Finally, antisense oligonucleotides of miR-222 transfection was used to silence miR-222 in 3T3-L1 adipocytes. The results showed that the expressions of ERα and GLUT4, the insulin-stimulated translocation of GLUT4 from the cytoplasm to the cell membrane and glucose uptake in mature adipocytes were dramatically increased (P < .01). In conclusion, miR-222 is a potential regulator of ERα expression in estrogen-induced insulin resistance in GDM and might be a candidate biomarker and therapeutic target for GDM.

IntroductionPre-eclampsia (PE), a severe pregnancy-specific disease characterized by the new onset of hypertension, proteinuria, edema, and a series of other systematic disorders, is a state of widespread mitochondrial dysfunction of the placenta.MethodsWe compared the morphology of mitochondria in pre-eclamptic and normotensive placentae using electron microscopy. To reveal the systematic protein expression changes of placental mitochondria that might explain the pathogenesis of PE, we performed iTRAQ analysis combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS) on differentially expressed placental mitochondria proteins from 4 normotensive and 4 pre-eclamptic pregnancies. Bioinformatics analysis was used to find the relative processes that these differentially expressed proteins were involved in. Three differentially expressed proteins were chosen to confirm by Western blotting and immunohistochemistry.ResultsMorphological data demonstrated degenerative and apoptotic changes in the mitochondria of pre-eclamptic placentae. We found four proteins were upregulated and 22 proteins were downregulated in pre-eclamptic placentae compared with normotensive placentae. Bioinformatics analysis showed that these proteins were involved in many critical processes in the development of pre-eclampsia such as apoptosis, fatty acid oxidation, the respiratory chain, reactive oxygen species generation, the tricarboxylic acid cycle and oxidative stress.ConclusionsThis preliminary work provides a better understanding of the proteomic alterations of mitochondria from pre-eclamptic placentae and may aid in our understanding of the importance of mitochondria in the development of pre-eclampsia.

These observations suggested that several subtypes of the AQP family play a role in human breast carcinogenesis.

Genomic imprinting is an epigenetic phenomenon by which certain genes display differential expression in a parent-of-origin-dependent manner. Hundreds of imprinted genes have been identified from several plant species. Here, we identified, with a high level of confidence, 208 imprinted gene candidates from rice (). Imprinted genes of rice showed limited association with the transposable elements, which contrasts with findings from Arabidopsis (). Generally, imprinting in rice is conserved within a species, but intraspecific variation also was detected. The imprinted rice genes do not show signatures of selection, which suggests that domestication has had a limited evolutionary consequence on genomic imprinting. Although conservation of imprinting in plants is limited, we show that some loci are imprinted in several different species. Moreover, our results suggest that different types of epigenetic regulation can be established either before or after fertilization. Imprinted 24-nucleotide small RNAs and their neighboring genes tend to express alleles from different parents. This association was not observed between 21-nucleotide small RNAs and their neighboring genes. Together, our findings suggest that the regulation of imprinting can be diverse, and genomic imprinting has evolutionary and biological significance.

The mature oocyte contains the full complement of maternal proteins required for fertilization, the transition to zygotic transcription, and the beginning stages of embryogenesis. Many of these proteins have yet to be characterized. In this study, two-dimensional electrophoresis (2-DE) of mouse metaphase-II (MII) oocyte proteins, stained with silver staining or Pro-Q Diamond dye, was performed to describe the proteome and phosphoproteome of the mouse oocyte derived from ICR mice. A total of 869 selected protein spots, corresponding to 380 unique proteins, were identified successfully by mass spectrometry, in which 90 protein spots representing 53 unique proteins have been stained with Pro-Q Diamond, indicating that they are in phosphorylated forms. All identified proteins were bioinformatically annotated in detail and compared with the embryonic stem cell (ESC) proteome. A proteome reference database for the mouse oocyte was established from the protein data generated in this study, which can be accessed over the Internet ( http://reprod.njmu.edu.cn/2d). This database is the most detailed mouse oocyte proteomic database to date. It should be valuable in expanding our knowledge of the regulation of signaling in oogenesis, fertilization, and embryo development, while revealing potential mechanisms for epigenetic reprogramming.

Aims/Introduction: To investigate the changes in the gut microbiome in the second trimester of pregnancy associated with later-diagnosed gestational diabetes mellitus (GDM) and their relationship with fasting serum levels of metabolites, especially glucose. Materials and Methods: We carried out a case-control study with 110 GDM patients and 220 healthy pregnant women who provided fecal samples for 16S ribosomal ribonucleic acid sequencing in the second trimester of pregnancy. Results: Our results showed that GDM patients had lower a-diversity that was significantly associated with glycemic traits. Principal coordinates analysis showed significantly different microbial communities, as within GDM patients, seven genera within the phylum Firmicutes and two within the phylum Actinobacteria were significantly decreased, and four genera within phylum Bacteroidetes were increased. In addition, microbiota co-occurrence network analysis was carried out, and decreased genera within the phylum Firmicutes in GDM patients showed a significant negative correlation with oral glucose tolerance test values. Finally, microbial gene functions related to glycan biosynthesis and metabolism were found to be enriched in GDM patients. Conclusions: Our results show the relationship between changed gut microbiota composition in the second trimester of pregnancy before the diagnosis of GDM and fasting serum levels of metabolites, which might inform the diagnosis, prevention and treatment of GDM.