In this study, the phytotoxicity of seven metal oxide nanoparticles(NPs)-titanium dioxide (nTiO₂), silicon dioxide (nSiO₂), cerium dioxide (nCeO₂), magnetite (nFe₃O₄), aluminum oxide (nAl₂O₃), zinc ...oxide (nZnO) and copper oxide (nCuO)-was assessed on two agriculturally significant crop plants (maize and rice). The results showed that seed germination was not affected by any of the seven metal oxide NPs. However, at the concentration of 2000 mg·L(-1), the root elongation was significantly inhibited by nCuO (95.73% for maize and 97.28% for rice), nZnO (50.45% for maize and 66.75% for rice). On the contrary, minor phytotoxicity of nAl₂O₃ was only observed in maize, and no obvious toxic effects were found in the other four metal oxide NPs. By further study we found that the phytotoxic effects of nZnO, nAl₂O₃ and nCuO (25 to 2000 mg·L(-)¹) were concentration dependent, and were not caused by the corresponding Cu(2+), Zn(2+) and Al(3+) ions (0.11 mg·L(-)¹, 1.27 mg·L(-)¹ and 0.74 mg·L(-)¹, respectively). Furthermore, ZnO NPs (<50 nm) showed greater toxicity than ZnO microparticles(MPs)(<5 μm) to root elongation of both maize and rice. Overall, this study provided valuable information for the application of engineered NPs in agriculture and the assessment of the potential environmental risks.
This work focused on the toxicity evaluation of ZnO NPs and their uptake and transportation in a significant crop plant, Rice (Oryza sativa L.). Under hydroponic condition, 25, 50 and 100 mg/L ZnO ...NPs could inhibit the growth of rice seedlings by reducing their biomass comparing with Zn2+ (13.82 mg/L) treatment and the control. In addition, physiological index was determined, involving the decrease of the chlorophyll content, which was further confirmed by the down-regulation of photosynthetic pigment related genes. Based on the expression levels of the genes encoding three antioxidant enzyme, e.g. Catalase (EC 1.11.1.6), Ascorbate peroxidase (EC 1.11.1.11) and Superoxide dismutase (EC 1.15.1.1), the oxidative damage was found in ZnO NPs exposed rice. On the other hand, by ultra-thin slicing and transmission electron microscopy, ZnO NPs were observed in the intercellular space and cytoplasm of rice root cells, and their transport to aerial tissue from roots were further confirmed by inductively coupled plasma atomic emission spectrometer. Overall, ZnO NPs could be uptaken by rice in the form of ions or particles, which further affected plant growth and development at phenotypic, physiological and molecular levels.
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•The growth inhibition of rice seedlings by ZnO NPs was concentration dependent.•ZnO NPs could reduce the synthesis of chlorophylls in rice leaves.•ZnO NPs were found to induce the oxidative damage of rice.•ZnO NPs could be absorbed by rice roots and further transported to aerial tissue.
Coronary arteries bring blood flow to the heart muscle. Understanding the developmental program of the coronary arteries provides insights into the treatment of coronary artery diseases. Multiple ...sources have been described as contributing to coronary arteries including the proepicardium, sinus venosus （SV）, and endocardium. However, the developmental origins of coronary vessels are still under intense study. We have produced a new genetic tool for studying coronary development, an AplnCreER mouse line, which expresses an inducible Cre recombinase specifically in developing coronary vessels. Quantitative analysis of coronary development and timed induction of AplnCreER fate tracing showed that the progenies of subepicardial endothelial cells （ECs） both invade the compact myocardium to form coronary arteries and remain on the surface to produce veins. We found that these subepicardial ECs are the major sources of intramyocardial coronary vessels in the developing heart. In vitro explant assays indicate that the majority of these subepicardial ECs arise from endocardium of the SV and atrium, but not from ventricular endocardium. Clonal analysis of Apln-positive cells indicates that a single subepicardial EC contributes equally to both coronary arteries and veins. Collectively, these data suggested that subepieardial ECs are the major source of intramyocardial coronary arteries in the ventricle wall, and that coronary arteries and veins have a common origin in the developing heart.
Macrophages acquire distinct phenotypes during tissue stress and inflammatory responses, but the mechanisms that regulate the macrophage polarization are poorly defined. Here we show that tuberous ...sclerosis complex 1 (TSC1) is a critical regulator of M1 and M2 phenotypes of macrophages. Mice with myeloid-specific deletion of TSC1 exhibit enhanced M1 response and spontaneously develop M1-related inflammatory disorders. However, TSC1-deficient mice are highly resistant to M2-polarized allergic asthma. Inhibition of the mammalian target of rapamycin (mTOR) fails to reverse the hypersensitive M1 response of TSC1-deficient macrophages, but efficiently rescues the defective M2 polarization. Deletion of mTOR also fails to reverse the enhanced inflammatory response of TSC1-deficient macrophages. Molecular studies indicate that TSC1 inhibits M1 polarization by suppressing the Ras GTPase-Raf1-MEK-ERK pathway in mTOR-independent manner, whereas TSC1 promotes M2 properties by mTOR-dependent CCAAT/enhancer-binding protein-β pathways. Overall, these findings define a key role for TSC1 in orchestrating macrophage polarization via mTOR-dependent and independent pathways.
Lipid transport and ATP synthesis are critical for the progression of non-alcoholic fatty liver disease (NAFLD), but the underlying mechanisms are largely unknown. Here, we report that the ...RNA-binding protein HuR (ELAVL1) forms complexes with NAFLD-relevant transcripts. It associates with intron 24 of Apob pre-mRNA, with the 3'UTR of Uqcrb, and with the 5'UTR of Ndufb6 mRNA, thereby regulating the splicing of Apob mRNA and the translation of UQCRB and NDUFB6. Hepatocyte-specific HuR knockout reduces the expression of APOB, UQCRB, and NDUFB6 in mice, reducing liver lipid transport and ATP synthesis, and aggravating high-fat diet (HFD)-induced NAFLD. Adenovirus-mediated re-expression of HuR in hepatocytes rescues the effect of HuR knockout in HFD-induced NAFLD. Our findings highlight a critical role of HuR in regulating lipid transport and ATP synthesis.
Diabetic cardiomyopathy is a progressive disease in diabetic patients, and myocardial insulin resistance contributes to its pathogenesis through incompletely-defined mechanisms. Striated muscle ...preferentially expressed protein kinase (SPEG) has two kinase-domains and is a critical cardiac regulator. Here we show that SPEG is phosphorylated on Ser
/Ser
/Thr
by protein kinase B (PKB) in response to insulin. PKB-mediated phosphorylation of SPEG activates its second kinase-domain, which in turn phosphorylates sarcoplasmic/endoplasmic reticulum calcium-ATPase 2a (SERCA2a) and accelerates calcium re-uptake into the SR. Cardiac-specific deletion of PKBα/β or a high fat diet inhibits insulin-induced phosphorylation of SPEG and SERCA2a, prolongs SR re-uptake of calcium, and impairs cardiac function. Mice bearing a Speg
mutation to prevent its phosphorylation by PKB display cardiac dysfunction. Importantly, the Speg
mutation impairs SERCA2a phosphorylation and calcium re-uptake into the SR. Collectively, these data demonstrate that insulin resistance impairs this PKB-SPEG-SERCA2a signal axis, which contributes to the development of diabetic cardiomyopathy.
E4BP4, a circadian protein, is indispensable for NK cell development. It remains largely unknown which signal is required to induce E4BP4 expression and what effects it has during NK cell ...differentiation. Here, we reveal that PDK1, a kinase upstream of mTOR, connects IL-15 signaling to E4BP4. Early deletion of PDK1 caused a severe loss of NK cells and compromised antitumor activity in vivo. PDK1-deficient NK cells displayed much weaker IL-15-induced mTOR activation and E4BP4 induction, as well as remarkable reduction in CD122, a receptor subunit specifying NK cell responsiveness to IL-15. The phenotypes were partially reversible by ectopic expression of E4BP4 or bypassed activation of mTOR. We also determined that PDK1-mediated metabolic signaling was dispensable for NK cell terminal maturation and survival. Thus, we identify a role for PDK1 signaling as a key mediator in regulating E4BP4 expression during early NK cell development. Our findings underscore the importance of IL-15 self-responsiveness through a positive feedback loop that involves PDK1-mTOR-E4BP4-CD122 signaling.
Key message
A gene controlling golden flesh trait in watermelon was discovered and fine mapped to a 39.08 Kb region on chromosome 1 through a forward genetic strategy, and Cla97C01G008760 (annotated ...as phytoene synthase protein, ClPsy1 ) was recognized as the most likely candidate gene.
Vitamin A deficiency is a worldwide public nutrition problem, and β-carotene is the precursor for vitamin A synthesis. Watermelon with golden flesh (gf, which occurs due to an accumulated abundance of β-carotene) is an important germplasm resource. In this study, a genetic analysis of segregated
gf
gene populations indicated that
gf
was controlled by a single recessive gene. BSA-seq (Bulked segregation analysis) and an initial linkage analysis placed the
gf
locus in a 290-Kb region on watermelon chromosome 1. Further fine mapping in a large population including over 1000 F
2
plants narrowed this region to 39.08 Kb harboring two genes,
Cla97C01G008760
and
Cla97C01G008770
, which encode phytoene synthase (
ClPsy1
) and GATA zinc finger domain-containing protein, respectively. Gene sequence alignment and expression analysis between parental lines revealed
Cla97C01G008760
as the best possible candidate gene for the gf trait. Nonsynonymous SNP mutations in the first exon of
ClPsy1
between parental lines co-segregated with the gf trait only among individuals in the genetic population and were not related to flesh color in natural watermelon panels. Promoter sequence analysis of 26 watermelon accessions revealed two SNPs in the
cis
-acting element sequences corresponding to MYB and MYC2 transcription factors. RNA-seq data and qRT-PCR verification showed that two MYBs exhibited expression trends similar to that of
ClPsy1
in the parental lines and may regulate the
ClPsy1
expression. Further research findings indicate that the gf trait is determined not only by
ClPsy1
but also by
ClLCYB
,
ClCRTISO
and
ClNCED7
, which play important roles in watermelon β-carotene accumulation.
• Floral flavonols play specific pivotal roles in pollinator attraction, pollen germination and fertility, in addition to other functions in vegetative organs. For many plants, the process of ...flavonol biosynthesis in late flower development stages and in mature flower tissues is poorly understood, in contrast to early flower development stages. It is thought that this process may be regulated independently of subgroup 7 R2R3 MYB (SG7 MYB) transcription factors.
• In this study, two FLS genes were shown to be expressed synchronously with the flower development-specific and tissue-specific biosynthesis of flavonols in Freesia hybrida.
• FhFLS1 contributed to flavonol biosynthesis in early flower buds, toruses and calyxes, and was regulated by four well-known SG7 MYB proteins, designated as FhMYBFs, with at least partial regulatory redundancy. FhFLS2 accounted for flavonols in late developed flowers and in the petals, stamens and pistils, and was targeted directly by non SG7 MYB protein FhMYB21L2. In parallel, AtMYB21 and AtMYB24 also activated AtFLS1, a gene highly expressed in Arabidopsis anthers and pollen, indicating the conserved regulatory roles of MYB21 against FLS genes in these two evolutionarily divergent angiosperm plants.
• Our results reveal a novel regulatory and synthetic mechanism underlying flavonol biosynthesis in floral organs and tissues which may be exploited to investigate supplementary roles of flavonols in flowers.
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