Excess centrosomes perturb dynamic endothelial cell repolarization during blood vessel formation

Blood vessel formation requires dynamic movements of endothelial cells (ECs) within sprouts. The cytoskeleton regulates migratory polarity, and centrosomes organize the microtubule cytoskeleton. However, it is not well understood how excess centrosomes, commonly found in tumor stromal cells, affect microtubule dynamics and interphase cell polarity. Here we find that ECs dynamically repolarize during sprouting angiogenesis, and excess centrosomes block repolarization and reduce migration and sprouting. ECs with excess centrosomes initially had more centrosome-derived microtubules but, paradoxically, fewer steady-state microtubules. ECs with excess centrosomes had elevated Rac1 activity, and repolarization was rescued by blockade of Rac1 or actomyosin blockers, consistent with Rac1 activity promoting cortical retrograde actin flow and actomyosin contractility, which precludes cortical microtubule engagement necessary for dynamic repolarization. Thus normal centrosome numbers are required for dynamic repolarization and migration of sprouting ECs that contribute to blood vessel formation

Approaching the Intrinsic Bandgap in Suspended High-Mobility Graphene Nanoribbons

We report electrical transport measurements on a suspended ultra-low-disorder graphene nanoribbon(GNR) with nearly atomically smooth edges that reveal a high mobility exceeding 3000 cm2 V-1 s-1 and an intrinsic band gap. The experimentally derived bandgap is in quantitative agreement with the results of our electronic-structure calculations on chiral GNRs with comparable width taking into account the electron-electron interactions, indicating that the origin of the bandgap in non-armchair GNRs is partially due to the magnetic zigzag edges.Comment: 22 pages, 6 figure

Tortuous Microvessels Contribute to Wound Healing via Sprouting AngiogenesisHighlights

Wound healing is accompanied by neoangiogenesis, and new vessels are thought to originate primarily from the microcirculation; however, how these vessels form and resolve during wound healing is poorly understood. Here, we investigated properties of the smallest capillaries during wound healing to determine their spatial organization and the kinetics of formation and resolution

All silicon passive addressed micro LED displays with nano-porous Si/ITO-free nanomesh layers as light emitting pixels

In this paper we will concentrate on the usage of novel technologies and nanostructured materials to fabricate low cost high efficient micro LED displays with unique features. Possible areas of application will be discussed as well

Characterization and plant expression of glyphosate-tolerant enolpyruvylshikimate phosphate synthase

Abstract BACKGROUND: Glyphosate tolerance is a dominant trait in modern biotech crops. RESULTS: A gene encoding a glyphosate-tolerant EPSP synthase (aroA 1398 ) from bacterial strain ATX1398 was cloned and characterized. The protein is initiated at a GTG translational start codon to produce a protein that provides robust glyphosate resistance in Escherichia coli (Mig) Cast & Chalm. The aroA 1398 protein was expressed and purified from E. coli, and key kinetic values were determined (K i = 161 µM; K m (PEP) = 11.3 µM; k cat = 28.3 s −1 ). The full-length enzyme is 800-fold more resistant to glyphosate than the maize EPSP synthase while retaining high affinity for the substrate phosphoenol pyruvate. To evaluate further the potential of aroA 1398 , transgenic maize events expressing the aroA 1398 protein were generated. T 0 plants were screened for tolerance to glyphosate sprays at 1.3× commercial spray rates, and T 1 plants were selected that completely resisted glyphosate sprays at 1×, 2× and 4× recommended spray rates in field trials. CONCLUSION: These data suggest that aroA 1398 is a suitable candidate for conferring glyphosate tolerance in transgenic crop plants

Tumor-Derived Factors and Reduced p53 Promote Endothelial Cell Centrosome Over-Duplication

<div><p>Approximately 30% of tumor endothelial cells have over-duplicated (>2) centrosomes, which may contribute to abnormal vessel function and drug resistance. Elevated levels of vascular endothelial growth factor A induce excess centrosomes in endothelial cells, but how other features of the tumor environment affect centrosome over-duplication is not known. To test this, we treated endothelial cells with tumor-derived factors, hypoxia, or reduced p53, and assessed centrosome numbers. We found that hypoxia and elevated levels of bone morphogenetic protein 2, 6 and 7 induced excess centrosomes in endothelial cells through BMPR1A and likely via SMAD signaling. In contrast, inflammatory mediators IL-8 and lipopolysaccharide did not induce excess centrosomes. Finally, down-regulation in endothelial cells of p53, a critical regulator of DNA damage and proliferation, caused centrosome over-duplication. Our findings suggest that some tumor-derived factors and genetic changes in endothelial cells contribute to excess centrosomes in tumor endothelial cells.</p></div