FLOURY ENDOSPERM6 encodes a CBM48 domain‐containing protein involved in compound granule formation and starch synthesis in rice endosperm

Starch is the most widespread form of energy storage in the plant kingdom. Although many enzymes and related factors have been identified for starch biosynthesis, unknown players remain to be identified, given that it is a complicated and sophisticated process. The endosperm of rice (Oryza sativa) has been used for the study of starch synthesis. Here, we report the cloning and characterization of the FLOURY ENDOSPERM6 (FLO6) gene in rice. In the flo6 mutant, the starch content is decreased and the normal physicochemical features of starch are changed. Significantly, flo6 mutant endosperm cells show obvious defects in compound granule formation. Map‐based cloning showed that FLO6 encodes a protein of unknown function. It harbors an N–terminal transit peptide that ensures its correct localization and functions in the plastid, and a C–terminal carbohydrate‐binding module 48 (CBM48) domain that binds to starch. Furthermore, FLO6 can interact with isoamylase1 (ISA1) both in vitro and in vivo, whereas ISA1 does not bind to starch directly. We thus propose that FLO6 may act as a starch‐binding protein involved in starch synthesis and compound granule formation through a direct interaction with ISA1 in developing rice seeds. Our data provide a novel insight into the role of proteins with the CBM48 domain in plant species.     

Mequindox induced cellular DNA damage via generation of reactive oxygen species

Mequindox, a quinoxaline-N-dioxide derivative that possesses antibacterial properties, has been widely used as a feed additive in the stockbreeding industry in China. While recent pharmacological studies have uncovered potential hazardous effects of mequindox, exactly how mequindox induces pathological changes and the cellular responses associated with its consumption remain largely unexplored. In this study, we investigated the cellular responses associated with mequindox treatment. We report here that mequindox inhibits cell proliferation by arresting cells at the G2/M phase of the cell cycle. Interestingly, this mequindox-associated deleterious effect on cell proliferation was observed in human, pig as well as chicken cells, suggesting that mequindox acts on evolutionarily conserved target(s). To further understand the mequindox-host interaction and the mechanism underlying mequindox-induced cell cycle arrest, we measured the cellular content of DNA damage, which is known to perturb cell proliferation and compromise cell survival. Accordingly, using γ-H2AX as a surrogate marker for DNA damage, we found that mequindox treatment induced cellular DNA damage, which paralleled the chemical-induced elevation of reactive oxygen species (ROS) levels. Importantly, expression of the antioxidant enzyme catalase partially alleviated these mequindox-associated effects. Taken together, our results suggest that mequindox cytotoxicity is attributable, in part, to its role as a potent inducer of DNA damage via ROS.     

A Cotton Annexin Protein AnxGb6 Regulates Fiber Elongation through Its Interaction with Actin 1

Annexins are assumed to be involved in regulating cotton fiber elongation, but direct evidence remains to be presented. Here we cloned six Annexin genes (AnxGb) abundantly expressed in fiber from sea-island cotton (G. barbadense). qRT-PCR results indicated that all six G. barbadense annexin genes were expressed in elongating cotton fibers, while only the expression of AnxGb6 was cotton fiber-specific. Yeast two hybridization and BiFC analysis revealed that AnxGb6 homodimer interacted with a cotton fiber specific actin GbAct1. Ectopic-expressed AnxGb6 in Arabidopsis enhanced its root elongation without increasing the root cell number. Ectopic AnxGb6 expression resulted in more F-actin accumulation in the basal part of the root cell elongation zone. Analysis of AnxGb6 expression in three cotton genotypes with different fiber length confirmed that AnxGb6 expression was correlated to cotton fiber length, especially fiber elongation rate. Our results demonstrated that AnxGb6 was important for fiber elongation by potentially providing a domain for F-actin organization.     

Insulin and Chromium Picolinate Induce Translocation of CD36 to the Plasma Membrane Through Different Signaling Pathways in 3T3-L1 Adipocytes,and with a Differential Functionality of the CD36

Chromium picolinate (CrPic) has been indicated to activate glucose transporter 4 (GLUT4) trafficking to the plasma membrane (PM) to enhance glucose uptake in 3T3-L1 adipocytes. In skeletal and heart muscle cells, insulin directs the intracellular trafficking of the fatty acid translocase/CD36 to induce the uptake of cellular long-chain fatty acid (LCFA). The current study describes the effects of CrPic and insulin on the translocation of CD36 from intracellular storage pools to the PM in 3T3-L1 adipocytes in comparison with that of GLUT4. Immunofluorescence microscopy and immunoblotting revealed that both CD36 and GLUT4 were expressed and primarily located intracellularly in 3T3-L1 adipocytes. Upon insulin or CrPic stimulation, PM expression of CD36 increased in a similar manner as that for GLUT4; the CrPic-stimulated PM expression was less strong than that of insulin. The increase in PM localization for these two proteins by insulin paralleled LCFA ([1-¹⁴C]palmitate) or [³H]deoxyglucose uptake in 3T3-L1 adipocytes. The induction of the PM expression of GLUT4, but not CD36, or substrate uptake by insulin and CrPic appears to be additive in adipocytes. Furthermore, wortmannin completely inhibited the insulin-stimulated translocation of GLUT4 or CD36 and prevented the increased uptake of glucose or LCFA in these cells. Taken together, for the first time, these findings suggest that both insulin and CrPic induce CD36 translocation to the PM in 3T3-L1 adipocytes and that their translocation-inducing effects are not additive. The signaling pathway inducing the translocations is different, apparently resulting in a differential activity of CD36.     

Round fruit shape in WI7239 cucumber is controlled by two interacting quantitative trait loci with one putatively encoding a tomato <Emphasis Type="Italic">SUN</Emphasis> homolog

Key message

QTL analysis revealed two interacting loci, FS1.2 and FS2.1, underlying round fruit shape in WI7239 cucumber; CsSUN , a homolog of tomato fruit shape gene SUN , was a candidate for FS1.2.

Abstract

Fruit size is an important quality and yield trait in cucumber, but its genetic basis remains poorly understood. Here we reported QTL mapping results on fruit size with segregating populations derived from the cross between WI7238 (long fruit) and WI7239 (round fruit) inbred cucumber lines. Phenotypic data of fruit length and diameter were collected at anthesis, immature and mature fruit stages in four environments. Ten major-effect QTL were detected for six traits; synthesis of information from these QTL supported two genes, FS1.2 and FS2.1, underlying fruit size variation in the examined populations. Under the two-gene model, deviation from expected segregation ratio in fruit length and diameter among segregating populations was observed, which could be explained mainly by the interactions between FS1.2 and FS2.1, and segregation distortion in the FS2.1 region. Genome-wide candidate gene search identified CsSUN, a homolog of the tomato fruit shape gene SUN, as the candidate for FS1.2. The round-fruited WI7239 had a 161-bp deletion in the first exon of CsSUN, and its expression in WI7239 was significantly lower than that in WI7238. A marker derived from this deletion was mapped at the peak location of FS1.2 in QTL analysis. Comparative analysis suggested the melon gene CmSUN-14, a homolog of CsSUN as a candidate of the fl2/fd2/fw2 QTL in melon. This study revealed the unique genetic architecture of round fruit shape in WI7239 cucumber. It also highlights the power of QTL analysis for traits with a simple genetic basis but their expression is complicated by other factors.

     

A Dopant‐Free Polymeric Hole‐Transporting Material Enabled High Fill Factor Over 81% for Highly Efficient Perovskite Solar Cells

Although perovskite solar cells (PVSCs) have achieved rapid progress in the past few years, most of the high‐performance device results are based on the doped small molecule hole‐transporting material (HTM), spiro‐OMeTAD, which affects their long‐term stability. In addition, some defects from under‐coordinated Pb atoms on the surface of perovskite films can also result in nonradiative recombination to affect device performance. To alleviate these problems, a dopant‐free HTM based on a donor‐acceptor polymer, PBT1‐C, synthesized from the copolymerization between the benzodithiophene and 1,3‐bis(4‐(2‐ethylhexyl)thiophen‐2‐yl)‐5,7‐bis(2‐alkyl)benzo[1,2‐c:4,5‐c′]dithiophene‐4,8‐dione units is introduced. PBT1‐C not only possesses excellent hole mobility, but is also able to passivate the surface traps of the perovskite films. The derived PVSC shows a high power conversion efficiency of 19.06% with a very high fill factor of 81.22%, which is the highest reported for dopant‐free polymeric HTMs. The results from photoluminescence and trap density of states measurements validate that PBT1‐C can effectively passivate both surface and grain boundary traps of the perovskite.     

Phosphatidylserine Synthase Controls Cell Elongation Especially in the Uppermost Internode in Rice by Regulation of Exocytosis

The uppermost internode is one of the fastest elongating organs in rice, and is expected to require an adequate supply of cell-wall materials and enzymes to the cell surface to enhance mechanical strength. Although it has been reported that the phenotype of shortened uppermost internode 1 (sui1) is caused by mutations in PHOSPHATIDYLSERINE SYNTHASE (OsPSS), the underlying mechanism remains unclear. Here we show that the OsPSS-1, as a gene expressed predominantly in elongating cells, regulates post-Golgi vesicle secretion to intercellular spaces. Mutation of OsPSS-1 leads to compromised delivery of CESA4 and secGFP towards the cell surface, resulting in weakened intercellular adhesion and disorganized cell arrangement in parenchyma. The phenotype of sui1-4 is caused largely by the reduction in cellulose contents in the whole plant and detrimental delivery of pectins in the uppermost internode. We found that OsPSS-1 and its potential product PS (phosphatidylserine) localized to organelles associated with exocytosis. These results together suggest that OsPSS-1 plays a potential role in mediating cell expansion by regulating secretion of cell wall components.     

Study on the purification and chemical compositions of tea glycoprotein

In this paper, improvement in the method for purifying glycoprotein from green tea (Camellia sinensis) was described; some properties and chemical compositions of tea glycoprotein (TGP) were determined by HPGPC, FT-IR, GC–MS technologies. Compared to existing methods, a more compatible method for purifying TGP was proposed. This method was faster, simpler, more effective and easier to be extended to the industrial production than the method that used in our previous work. The molecular weight of TGP was 126,513 Da using HPGPC. GC–MS analysis of TGP showed that TGP was composed of seven kinds of monosaccharides, namely ribose, rhamnose, arabinose, xylose, mannose, glucose, galactose in molar ratios of 1.71:5.88:13.70:1.99:1.00:1.84:33.75. Eighteen amino acids were identified in TGP by amino acid analysis. The FT-IR spectrum of the TGP revealed also typical characteristics of polysaccharides, protein and uronic acid.