Polysaccharides constitute a major component of bacterial cell surfaces and play critical roles in bacteria/host interactions. The biosynthesis of such molecules, however, has mainly been characterized through in vivo genetic studies, thus precluding discernment of the details of this pathway. Accordingly, we present a chemical approach which enabled reconstitution of the E. coli O-polysaccharide biosynthetic pathway in vitro. Starting with chemically prepared N-Acetyl-D-galactosamine-diphospho-undecaprenyl, the E. coli O86 oligosaccharide repeating unit was assembled via sequential enzymatic glycosylation. Successful expression of the putative polymerase Wzy via a chaperone co-expression system then allowed demonstration of polymerization in vitro using this substrate. Analysis of additional substrates revealed a defined mode of recognition for Wzy towards the lipid moiety. Specific polysaccharide chain length modality was furthermore demonstrated to result from the action of Wzz. Collectively, polysaccharide biosynthesis was chemically reconstituted in vitro, providing a well-defined system for further underpinning molecular details of this biosynthetic pathway.
A zirconium-based
metal–organic framework (MOF) was successfully
constructed via solvothermal assembly of a triphenylamine-based
tricarboxylate ligand and Zr(IV) salt, the structure simulation of
which revealed that it possesses a two-dimensional layered framework
with a relatively rare dodecnuclear Zr12 cluster as the
inorganic building unit. The inherent photo-responsive property derived
from the incorporated photochromic triphenylamine groups combined
with its high stability makes the constructed MOF an efficient heterogeneous
photocatalyst for the oxidation of sulfides, which is a fundamentally
important reaction type in both environmental and pharmaceutical industries.
The photocatalytic activity of the constructed MOF was first investigated
under various conditions with thioanisole as a representative sulfide
substrate. The MOF exhibited both high efficiency and selectivity
on aerobic oxidation of thioanisole in methanol utilizing molecular
oxygen in air as the oxidant under blue light irradiation for 10 h.
Its high photocatalytic performance was also observed when extending
the sulfide substrate to diverse thioanisole derivatives and even
a sulfur-containing nerve agent simulant (2-chloroethyl ethyl sulfide).
The high photocatalytic efficiency and selectivity to a broad set
of sulfide substrates make the triphenylamine-incorporating zirconium-based
MOF a highly promising heterogeneous photocatalyst.
Prenatal and postnatal over-nutrition has emerged as a new health issue contributing to metabolic disorders in early development of the offspring. Accumulating evidence has suggested that adverse prenatal and postnatal environments gave rise to the predisposition to metabolic syndromes including hyperglycemia, obesity, and diabetes. However, little research has concentrated on the effects of exposures to both adverse conditions before and after birth of the offspring. In this study, we aimed to investigate whether prenatal and postnatal over-nutrition is able to cause metabolic disorders to female mice feed on high-fat/fructose diet (HFFD) as well as their offspring. Female mice were fed on either HFFD or a normal chow diet (NC), while their offspring were divided into four experimental groups as NC/NC, HFFD/NC, NC/HFFD, and HFFD/HFFD (prenatal/postnatal diet order), respectively. Both NC/HFFD and HFFD/HFFD offspring exhibited obvious body weight and fat content gain, hyperglycemia, and severe insulin resistance. Interestingly, when compared to NC/HFFD offspring, the HFFD/HFFD offspring exhibited more severe alterations in their metabolism and dysfunctions on pancreatic β-cells, suggesting a potential impact of prenatal HFFD on the programming of pancreatic β-cell deficiency in the fetus. Meanwhile, the results from HFFD/NC mice indicated that a balance diet after birth partially compensated the adverse prenatal HFFD impact. In conclusion, this study demonstrated that prenatal and postnatal over-nutrition increases severity of islet injury, hyperglycemia, and metabolic disorders in the offspring.
Stathmin 1 (STMN1) is a biomarker in several types of neoplasms. It plays an important role in cell cycle progression, mitosis, signal transduction and cell migration. In ovaries, STMN1 is predominantly expressed in granulosa cells (GCs). However, little is known about the role of STMN1 in ovary. In this study, we demonstrated that STMN1 is overexpressed in GCs in patients with polycystic ovary syndrome (PCOS). In mouse primary GCs, the overexpression of STMN1 stimulated progesterone production, whereas knockdown of STMN1 decreased progesterone production. We also found that STMN1 positively regulates the expression of Star (steroidogenic acute regulatory protein) and Cyp11a1 (cytochrome P450 family 11 subfamily A member 1). Promoter and ChIP assays indicated that STMN1 increased the transcriptional activity of Star and Cyp11a1 by binding to their promoter regions. The data suggest that STMN1 mediates the progesterone production by modulating the promoter activity of Star and Cyp11a1. Together, our findings provide novel insights into the molecular mechanisms of STMN1 in ovary GC steroidogenesis. A better understanding of this potential interaction between STMN1 and Star in progesterone biosynthesis in GCs will facilitate the discovery of new therapeutic targets in PCOS.
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