Lifetime-Extending 3-(4-Phenylbenzo[4,5]thieno[3,2-d]pyrimidin-2-yl)benzonitrile Acceptor for Thermally Activated Delayed Fluorescence Emitters.

Highly efficient and long-living green thermally activated delayed fluorescence (TADF) organic light-emitting diodes (OLEDs) were developed using benzothienopyrimidine-4-benzonitrile acceptor-derived compounds as the TADF emitters. A molecular design merging the benzothienopyrimidine-4-benzonitrile acceptor with either indolocarbazole or diindolocarbazole was employed to prepare two TADF emitters, 5-(2-phenylbenzo[4,5]thieno[3,2-d]pyrimidin-4-yl)-2-(5-phenylindolo[3,2-a]carbazol-12(5H)-yl)benzonitrile and 2-(10,15-diphenyl-10,15-dihydro-5H-diindolo[3,2-a:3',2'-c]carbazol-5-yl)-5-(2-phenylbenzo[4,5]thieno[3,2-d]pyrimidin-4-yl)benzonitrile (BTPDIDCz), as the green and greenish-yellow emitters. Among the two emitters, BTPDIDCz with the diindolocarbazole donor combined with the benzothienopyrimidine-4-benzonitrile acceptor demonstrated a high external quantum efficiency of 24.5% and 3 times longer device lifetime than the state-of-the-art green emitter. This work proposed the potential of benzothienopyrimidine-4-benzonitrile as the acceptor for long lifetime in TADF emitters.

Rational Molecular Design Overcoming the Long Delayed Fluorescence Lifetime and Serious Efficiency Roll-Off in Blue Thermally Activated Delayed Fluorescent Devices.

Blue thermally activated delayed fluorescent (TADF) devices with short excited-state lifetime, high reverse intersystem crossing rate, and low-efficiency roll-off were developed by managing the molecular structure of donor-acceptor-type blue emitters. Three isomers of blue TADF emitters with a diphenyltriazine acceptor and three carbazole donors were synthesized. The position of the donor moieties in the phenyl linker connecting the donor and acceptor moieties was controlled to devise compounds with a short delayed fluorescence lifetime. A blue TADF emitter with three carbazole donors at 2-, 3-, and 4- positions of a phenyl linker shortened the excited state lifetime to 4.1 µs, showed a high external quantum efficiency of 20.4 %, and low efficiency roll-off of less than 10 % at 1000 cd m-2 . Therefore, a molecular design distorting the donors by aligning them in a consecutive way is useful to resolve the issues of long delayed fluorescence lifetime and efficiency roll-off of blue TADF devices.

Dihedral Angle Control of Blue Thermally Activated Delayed Fluorescent Emitters through Donor Substitution Position for Efficient Reverse Intersystem Crossing.

This study shows a molecular design strategy for controlling the dihedral angle of two carbazole donors linked to a 2,4-diphenyl-1,3,5-triazine acceptor by a phenyl unit. Using this approach, six thermally activated delayed fluorescence emitters were synthesized with donors placed in various positions around a central phenyl core, and the photophysical relationship between the donor position and its dihedral angle was investigated. We demonstrate that this angle can affect both the strength of the charge transfer state and the conjugation across the entire molecule, effectively changing the singlet-triplet energy gap of the system. We conclude that materials containing two substituted -ortho donors or one -ortho and an adjacent -meta have the smallest energy gaps and the shortest delayed fluorescence lifetimes. On the other hand, emitters with no -ortho substituted donors have larger energy gaps and slow-to-negligible delayed fluorescence. When applying these materials to organic light-emitting diodes, these blue-emitting devices have a range of electrical properties, the best producing efficiencies as high as 21.8% together with high resistance to roll-off that correlate with the reverse intersystem crossing rates obtained.

Simple heteroatom engineering for tuning the triplet energy of organometallic host materials for red, green and blue phosphorescent organic light-emitting diodes.

Triplet energy tuning from 2.48 eV to 2.94 eV by just a simple change of heteroatom in the ligand structure of Be complexes was studied using azole based triplet host materials. Three Be organometallic host materials with azole type ligands were synthesized and could be used as the host materials from red to deep blue phosphorescent organic light-emitting diodes. High quantum efficiency was obtained in red, green, blue and deep blue devices using the Be complexes. In particular, a high quantum efficiency of 26.1% was achieved in blue phosphorescent organic light-emitting diodes.

Regulation of long chain unsaturated fatty acid synthesis in yeast.

Saccharomyces cerevisiae forms monounsaturated fatty acids using the ER membrane-bound Delta-9 fatty acid desaturase, Ole1p, an enzyme system that forms a double bond in saturated fatty acyl CoA substrates. Ole1p is a chimeric protein consisting of an amino terminal desaturase domain fused to cytochrome b5. It catalyzes the formation of the double bond through an oxygen-dependent mechanism that requires reducing equivalents from NADH. These are transferred to the enzyme via NADH cytochrome b5 reductase to the Ole1p cytochrome b5 domain and then to the diiron-oxo catalytic center of the enzyme. The control of OLE1 gene expression appears to mediated through the ER membrane proteins Spt23p and Mga2p. N-terminal fragments of these proteins are released by an ubiquitin/proteasome mediated proteolysis system and translocated to the nucleus where they appear to act as transcription coactivators of OLE1. OLE1 is regulated through Spt23p and Mga2p by multiple systems that control its transcription and mRNA stability in response to diverse stimuli that include nutrient fatty acids, carbon source, metal ions and the availability of oxygen.

Candida albicans Spt23p controls the expression of the Ole1p Delta9 fatty acid desaturase and regulates unsaturated fatty acid biosynthesis.

In Saccharomyces cerevisiae the endoplasmic reticulum membrane proteins scSpt23p and scMga2p control the formation of unsaturated fatty acids by a mechanism that involves their release from the membrane by ubiquitin-mediated proteolysis. The resulting soluble polypeptides act as transcription activators that specifically control the expression of scOLE1, a gene that encodes scOle1p, a Delta9 fatty acid desaturase that forms cis-monounsaturated fatty acids (9Z-16:1 and 9Z-18:1) from saturated fatty acyl-CoA precursors. ScOle1p is the only long chain fatty acid desaturase in Saccharomyces and its membrane and storage lipids contain only saturated fatty acids and the monounsaturated products of that enzyme. Most other fungi, however, express multiple endoplasmic reticulum desaturases, including enzymes that form both mono- and polyunsaturated fatty acids. These typically include Delta12 and Delta15 enzymes that form the polyunsaturated species, 9Z,12Z-18:2, and 9Z,12Z,15Z-18:3, which are the most abundant fatty acids in membrane and storage lipids. An analysis of genomic DNA sequences shows that Candida albicans has a single homologue of the Saccharomyces scSPT23 and scMGA2 genes that we designate here as caSPT23. This study describes the characterization of the caSPT23 gene product and shows that it can repair the unsaturated fatty acid auxotrophy when it is expressed in a Saccharomyces scspt23Delta;scmga2Delta strain. In addition we show caSPT23 is essential for the expression of one of the two Delta9 desaturase homologues in Candida and potentially other functions associated with fatty acid metabolism.

Depletion of phosphatidylcholine in yeast induces shortening and increased saturation of the lipid acyl chains: evidence for regulation of intrinsic membrane curvature in a eukaryote.

To study the consequences of depleting the major membrane phospholipid phosphatidylcholine (PC), exponentially growing cells of a yeast cho2opi3 double deletion mutant were transferred from medium containing choline to choline-free medium. Cell growth did not cease until the PC level had dropped below 2% of total phospholipids after four to five generations. Increasing contents of phosphatidylethanolamine (PE) and phosphatidylinositol made up for the loss of PC. During PC depletion, the remaining PC was subject to acyl chain remodeling with monounsaturated species replacing diunsaturated species, as shown by mass spectrometry. The remodeling of PC did not require turnover by the SPO14-encoded phospholipase D. The changes in the PC species profile were found to reflect an overall shift in the cellular acyl chain composition that exhibited a 40% increase in the ratio of C16 over C18 acyl chains, and a 10% increase in the degree of saturation. The shift was stronger in the phospholipid than in the neutral lipid fraction and strongest in the species profile of PE. The shortening and increased saturation of the PE acyl chains were shown to decrease the nonbilayer propensity of PE. The results point to a regulatory mechanism in yeast that maintains intrinsic membrane curvature in an optimal range.

Regulation of unsaturated fatty acid biosynthesis in Saccharomyces: the endoplasmic reticulum membrane protein, Mga2p, a transcription activator of the OLE1 gene, regulates the stability of the OLE1 mRNA through exosome-mediated mechanisms.

The Saccharomyces cerevisiae OLE1 gene encodes a membrane-bound Delta9 fatty-acid desaturase, whose expression is regulated through transcriptional and mRNA stability controls. In wild type cells grown on fatty acid-free medium, OLE1 mRNA has a half-life of 10 +/- 1.5 min (basal stability) that becomes highly unstable when cells are exposed to unsaturated fatty acids (regulated stability). Activation of OLE1 transcription is dependent on N-terminal fragments of two membrane proteins, Mga2p and Spt23p, that are proteolytically released from the membrane by a ubiquitin-mediated mechanism. Surprisingly, disruption of the MGA2 gene also reduces the half-life of the OLE1 transcript and abolishes fatty acid regulated instability. Disruption of its cognate, SPT23, has no effect on the half-life of the mRNA. Mga2p appears to have two distinct functions with respect to the OLE1 mRNA stability: a stabilizing effect in cells grown in fatty acid-free medium and a destabilizing function in cells that are exposed to unsaturated fatty acids. These functions are independent of OLE1 transcription and can confer basal and regulated stability on OLE1 mRNAs that are produced under the control of the unrelated GAL1 promoter. Expression of soluble, N-terminal fragments of Mga2p stabilize the transcript but do not confer fatty acid-regulated instability on the mRNA suggesting that the stabilizing functions of Mga2p do not require membrane processing and that modifications to the protein introduced during proteolysis may play a role in the destabilizing effect. An analysis of mutants that are defective in mRNA degradation indicate that the Mga2p-requiring control mechanism that regulates the fatty acid-mediated instability of the OLE1 transcript acts by activating exosomal 3' --> 5'-exonuclease degradation activity.

Maintenance and regulation of mRNA stability of the Saccharomyces cerevisiae OLE1 gene requires multiple elements within the transcript that act through translation-independent mechanisms.

The Saccharomyces cerevisiae OLE1 gene encodes a membrane-bound Delta-9 fatty acid desaturase, whose expression is regulated by unsaturated fatty acids through both transcriptional and mRNA stability controls. In fatty acid-free medium, the mRNA has a half-life of 10 +/- 1.5 min (basal stability) that drops to 2 +/- 1.5 min when cells are exposed to unsaturated fatty acids (regulated stability). A deletion analysis of elements within the transcript revealed that the sequences within the protein-coding region that encode transmembrane sequences and a part of the cytochrome b5 domain are essential for the basal stability of the transcript. Deletion of any of the three essential elements produced unstable transcripts and loss of regulated instability. By contrast, substitution of the 3'-untranslated region with that of the stable PGK1 gene did not affect the basal stability of the transcript and did not block regulated decay. Given that Ole1p is a membrane-bound protein whose activities are a major determinant of membrane fluidity, we asked whether membrane-associated translation of the protein was essential for basal and regulated stability. Insertion of stop codons within the transcript that blocked either translation of the entire protein or parts of the protein required for co-translation insertion of Ole1p had no effect. We conclude that the basal and regulated stability of the OLE1 transcript is resistant to the nonsense-mediated decay pathway and that the essential protein-encoding elements for basal stability act cooperatively as stabilizing sequences through RNA-protein interactions via a translation-independent mechanism.

Mga2p processing by hypoxia and unsaturated fatty acids in Saccharomyces cerevisiae: impact on LORE-dependent gene expression.

In Saccharomyces cerevisiae, OLE1 encodes a delta9 fatty acid desaturase, an enzyme that plays a critical role in maintaining the correct ratio of saturated to monounsaturated fatty acids in the cell membrane. Previous studies have demonstrated that (i) OLE1 expression is repressed by unsaturated fatty acids (UFAs) and induced by low oxygen tension, (ii) a component of this regulation is mediated through the same low oxygen response element (LORE) in the OLE1 promoter, and (iii) Mga2p is involved in LORE-dependent hypoxic induction of OLE1. We now report that LORE-CYC1 basal promoter-lacZ fusion reporter assays demonstrate that UFAs repress the reporter expression under hypoxic conditions in a dose-dependent manner via LORE. Electrophoretic mobility shift assays show that UFAs repress the hypoxia-induced complex formation with LORE. Studies with a construct encoding a truncated form of Mga2p support the hypothesis that both hypoxia and UFA signals affect the processing of Mga2p and the UFA repression of OLE1 hypoxic induction is mediated through Mga2p. Data from Western blot assays provide evidence that under normoxic conditions, Mga2p processing produces approximately equimolar levels of the membrane-bound and processed forms and is unaffected by UFAs. Hypoxic induction of OLE1, however, is associated with increased processing of the protein, resulting in an approximately fivefold increase in the soluble active form that is counteracted by exposure of the cells to unsaturated fatty acids. Data from this study suggest that the Mga2p-LORE interaction plays an important role in OLE1 expression under both normoxic and hypoxic conditions.