12 research outputs found

    Ultrafast dynamics and interlayer thermal coupling of hot carriers in epitaxial graphene

    Full text link
    We report the first application of nondegenerate ultrafast pump-probe spectroscopy to investigate the dynamics of hot Dirac Fermions in epitaxial graphene. The DT spectra can be understood in terms of the effect of hot thermal carrier distributions on interband transitions with no electron-hole interaction. We also investigate the thermal coupling between carriers of doped and undoped layers. The coupling time is found to be below 500fs. (© 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/61906/1/470_ftp.pd

    Ultrafast electronic dynamics in unipolar n-doped indium gallium arsenide/gallium arsenide self-assembled quantum dots.

    Full text link
    Photodetectors based on intraband infrared absorption in the quantum dots have demonstrated improved performance over its quantum well counterpart by lower dark current, relative temperature insensitivity, and its ability for normal incidence operation. Various scattering processes, including phonon emission/absorption and carrier-carrier scattering, are critical in understanding device operation on the fundamental level. In previous studies, our group has investigated carrier dynamics in both low- and high-density regime. Ultrafast electron-hole scattering and the predicted phonon bottleneck effect in intrinsic quantum dots have been observed. Further examination on electron dynamics in unipolar structures is presented in this thesis. We used n-doped quantum dot in mid-infrared photodetector device structure to study the electron dynamics in unipolar structure. Differential transmission spectroscopy with mid-infrared intraband pump and optical interband probe was implemented to measure the electron dynamics directly without creating extra electron-hole pair, Electron relaxation after excitation was measured under various density and temperature conditions. Rapid capture into quantum dot within ∼ 10 ps was observed due to Auger-type electron-electron scattering. Intradot relaxation from the quantum dot excited state to the ground state was also observed on the time scale of 100 ps. With highly doped electron density in the structure, the inter-sublevel relaxation is dominated by Auger-type electron-electron scattering and the phonon bottleneck effect is circumvented. Nanosecond-scale recovery in larger-sized quantum dots was observed, not intrinsic to electron dynamics but due to band-bending and built-in voltage drift. An ensemble Monte Carlo simulation was also established to model the dynamics in quantum dots and in goad agreement with the experimental results. We presented a comprehensive picture of electron dynamics in the unipolar quantum dot structure. Although the phonon bottleneck is circumvented with high doped electron density, relaxation processes in unipolar quantum dots have been measured with time scales longer than that of bipolar systems. The results explain the operation principles of the quantum dot infrared photodetector on a microscopic level and provide basic understanding for future applications and designs.Ph.D.Applied SciencesCondensed matter physicsElectrical engineeringOpticsPure SciencesUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/126328/2/3238118.pd

    dBRWD3 Regulates Tissue Overgrowth and Ectopic Gene Expression Caused by Polycomb Group Mutations.

    No full text
    To maintain a particular cell fate, a unique set of genes should be expressed while another set is repressed. One way to repress gene expression is through Polycomb group (PcG) proteins that compact chromatin into a silent configuration. In addition to cell fate maintenance, PcG proteins also maintain normal cell physiology, for example cell cycle. In the absence of PcG, ectopic activation of the PcG-repressed genes leads to developmental defects and malignant tumors. Little is known about the molecular nature of ectopic gene expression; especially what differentiates expression of a given gene in the orthotopic tissue (orthotopic expression) and the ectopic expression of the same gene due to PcG mutations. Here we present that ectopic gene expression in PcG mutant cells specifically requires dBRWD3, a negative regulator of HIRA/Yemanuclein (YEM)-mediated histone variant H3.3 deposition. dBRWD3 mutations suppress both the ectopic gene expression and aberrant tissue overgrowth in PcG mutants through a YEM-dependent mechanism. Our findings identified dBRWD3 as a critical regulator that is uniquely required for ectopic gene expression and aberrant tissue overgrowth caused by PcG mutations

    Ectopic expression of <i>Antp</i> is more sensitive to partial knockdown of <i>Taf5</i>, <i>Taf7</i>, <i>Cdk7</i>, and <i>CycH</i>.

    No full text
    <p>(A) Suppression of <i>Pc</i> depletion-induced ectopic expression of <i>Ubx</i> by depletion of <i>Taf5</i>, <i>Taf7</i>, <i>Cdk7</i>, and <i>CycH</i>. Quantification of Ubx positive neuron number in the doubly depleted brains as indicated. (B) The orthotopic expression of <i>Ubx</i> in the doubly depleted ventral nerve cords as indicated. (C) The orthotopic expression of <i>Ubx</i> in control, <i>Taf5</i>, <i>Taf7</i>, <i>Cdk7</i>, and <i>CycH</i> depleted ventral nerve cords. *** indicates p<0.0001 by Student's t-test. ns. indicates not significant. (D) The Trx-induced Abd-B expression (arrows) in the <i>CycH</i> knockdown wings. (E and F) The orthotopic expression of <i>Antp</i> in the <i>CycH</i> knockdown (E), and the control (F) wings. (G and H) The Abd-B expression in wings over-expressing both <i>trx</i> and <i>CycH</i> (G) or <i>CycH</i> alone (H) under the control of <i>ms1096-GAL4</i>. (I) The orthotopic expression of <i>Antp</i> in the <i>CycH</i> over-expression wings. Scale bars indicate 20μm.</p

    dBRWD3 suppresses ectopic expression of <i>upd</i> and activation of the JAK-STAT pathway.

    No full text
    <p>(A-C) The <i>upd1</i> (A), <i>upd2</i> (B), and <i>upd3</i> (C) mRNA levels of mosaic eye brain complexes isolated from <i>wild type</i>, <i>Scm</i><sup><i>D1</i></sup>, and <i>Scm</i><sup><i>D1</i></sup>, <i>dBRWD3</i><sup><i>s5349</i></sup> as indicated. Data are shown as means ± S.D. *, **, *** indicate P<0.01, 0.001, 0.0001 respectively by Student's t-test, n = 4. (D) A schematic illustration of a 3<sup>rd</sup> instar eye imaginal disc. MF stands for morphogenic furrow. The red square indicates the region examined in the following experiments. (E-I) Upd3 levels (arrows) in <i>Scm</i><sup><i>D1</i></sup> mutant clones (E), <i>Scm</i><sup><i>D1</i></sup>, <i>dBRWD3</i><sup><i>s5349</i></sup> double-mutant clones (F), <i>wild-type</i> clones (G), <i>Sce</i><sup><i>1</i></sup> mutant clones (H), and <i>dBRWD3</i><sup><i>s5349</i></sup>, <i>Sce</i><sup><i>1</i></sup> double-mutant clones (I) generated in 3<sup>rd</sup> instar eye imaginal discs by <i>ey-flp</i> and marked by the absence of GFP. Scale bars indicate 50μm. (J) Orthotopic Upd3 levels (arrows) in <i>dBRWD3</i><sup><i>s5349</i></sup> mutant clones generated in 2<sup>nd</sup> instar larval imaginal eye discs marked by the absence of GFP. Scale bars indicate 50μm. (K) Quantification analyses of orthotopic Upd3 levels (arrows) in <i>dBRWD3</i><sup><i>s5349</i></sup> mutant clones. ns. indicates not significant. (L) A schematic illustration of a 3<sup>rd</sup> instar antennal imaginal disc. The red square indicates the region examined in the following experiments. (M) GFP levels (arrows) of the 10XSTAT-nls-GFP reporter in a <i>wild-type</i> disc. (N-P) GFP levels (arrows) of the 10XSTAT-nls-GFP reporter in <i>Scm</i><sup><i>D1</i></sup> mutant clones (N), <i>Scm</i><sup><i>D1</i></sup>, <i>dBRWD3</i><sup><i>s5349</i></sup> double-mutant clones (O), and <i>dBRWD3</i><sup><i>s5349</i></sup> mutant clones (P) generated in 3<sup>rd</sup> instar antennal imaginal discs by <i>ey-flp</i> and marked by the absence of the <i>ubi</i> promoter driven mof-RFP. Scale bars indicate 50μm.</p

    <i>dBRWD3</i><sup><i>s5349</i></sup> mutation suppresses ectopic expression of <i>Antp</i> in <i>Scm</i> <sup><i>D1</i></sup> or <i>Sce</i><sup><i>1</i></sup> mutant eye clones.

    No full text
    <p>(A) A schematic illustration of a 3<sup>rd</sup> instar eye imaginal disc. The red square indicates the region examined in the following experiments. (B-F) Antennapedia (Antp) levels (arrows) in <i>wild-type</i> clones (B), <i>Scm</i><sup><i>D1</i></sup> mutant clones (C), <i>Scm</i><sup><i>D1</i></sup>, <i>dBRWD3</i><sup><i>s5349</i></sup> double-mutant clones (D), <i>Sce</i><sup><i>1</i></sup> mutant clones (E), and <i>dBRWD3</i><sup><i>s5349</i></sup> <i>Sce</i><sup><i>1</i></sup> double-mutant clones (F) generated in the 3<sup>rd</sup> instar eye imaginal discs by <i>ey-flp</i> and marked by the absence of GFP. Scale bars indicate 50μm. (G) A schematic illustration of a 3<sup>rd</sup> instar wing imaginal disc. V and D stand for ventral and dorsal (marked by grey) compartments, respectively. (H) Antp levels (arrows) in a <i>wild-type</i> wing. (I) Antp levels (arrowheads) in <i>dBRWD3</i><sup><i>s5349</i></sup> mutant wing disc clones generated by <i>hs-flp</i> and marked by the absence of GFP. Scale bars indicate 50μm.</p
    corecore