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  1. Richard C. Lavin (11198639) ; Calvin Johnson (3440432) ; et al.
    2021
    Bild
  2. Nishiyama, Shogo ; Tamura, Motohide ; et al.
    2009
    academicJournal
  3. Thomas Kisby (10751512) ; Irene de Lázaro (276398) ; et al.
    2021
    unknown
  4. Thomas Kisby (10751512) ; Irene de Lázaro (276398) ; et al.
    2021
    unknown
  5. Thomas Kisby (10751512) ; Irene de Lázaro (276398) ; et al.
    2021
    unknown
  6. Figure 3. Exogenous autoinducers drive V. cholerae aggregation and HapR is required. ; Quantitation of aggregate volume fraction at 22 h for the ΔvpsL HCD QS-locked (HCD-locked), ΔvpsL LCD QS-locked (LCD-locked), CAI-1-responsive (± CAI-1), and AI-2-responsive (± AI-2 and boric acid) V. cholerae strains (A). Autoinducers or solvent controls were added at the time of inoculation. Concentrations used: CAI-1: 5 μM, AI-2: 1 μM, and boric acid: 100 μM. (B) Quantitation of aggregate volume fraction (black bars) and bioluminescence (gray bars) at 22 h for the CAI-1-responsive strain to which CAI-1 was added at T = 0 h and from 3 to 8 h at 1 h intervals. Also shown is bioluminescence quantified in a CAI-1-responsive strain harboring the cosmid pBB1 which carries the luxCDABE genes. RLU denotes relative lights units, defined as counts/min mL−1 per OD600. In A and B aggregate volume fraction was quantified in a strain harboring mKO constitutively expressed from the chromosome; quantitation of mean ± standard deviation (SD) (N=3 biological replicates). Representative cross-sections of the ΔvpsL HCD-locked (C), ΔvpsL ΔaphA HCD-locked (D), ΔvpsL ΔhapR HCD-locked (E), ΔvpsL ΔaphA ΔhapR HCD-locked (F), ΔvpsL LCD-locked (G), ΔvpsL ΔaphA LCD-locked (H), ΔvpsL ΔhapR LCD-locked (I), and ΔvpsL ΔaphA ΔhapR LCD-locked (J) V. cholerae strains following 22 h of growth. (C–J) Magnification: 10X; scale bar: 250 μm. All strains harbor mKO constitutively expressed from the chromosome. (K) Quantitation of aggregate volume fraction for samples in C–J. Shown are mean ± SD (N=3 biological replicates). The ΔvpsL ΔaphA LCD-locked strain appears to exhibit modest aggregation (H), possibly due to AphA repression of hapR transcription (Rutherford et al., 2011), but the level of aggregation is below the detection threshold employed in the segmenting analysis (K).
    2019
    unknown
  7. Ghinassi, F. ; Licandro, J. ; et al.
    2002
    academicJournal
  8. Halaczkiewicz, Marta
    In: All Graduate Theses and Dissertations, 2022
    Online academicJournal
  9. 2018
    unknown
  10. Figure 2. Rod signaling influences TH-positive cell number and dopamine levels through ipRGC-independent pathways. ; (A) Diagram depicting potential pathways by which light information could reach DACs (1. Via melanopsin signals relayed by ipRGCs, (2. Via rod signals relayed to DACs, (3. Via cone signals relayed to DACs, or (4. Via rod, cone, and/or melanopsin signals through ipRGC-dependent pathways. Dashed arrows represent indirect influence through multicellular circuits while solid arrows represent direct synaptic connectivity between subtypes. (B) Diagram depicting signaling pathways disrupted in MKO, RKO, CKO, and DTA mouse lines. Dashed arrows represent indirect influence through multicellular circuits while solid arrows represent direct synaptic connectivity between subtypes. (C–D) TH+ cell number and DA levels in Control (black circles, n = 9), MKO (blue circles, n = 6), RKO (red circles, n = 8), and CKO (green circles, n = 9) retinas from adult littermates. (E–F) TH+ cell number (n = 8 Control, n = 6 DTA) and DA levels (n = 6 Control, n = 6 DTA) in Control (black circles) and DTA (gray circles) retinas from adult littermates. (G) TH+ cell anatomy in WT and DTA adult retinal sections. We observed no morphological differences between TH+ cells in these two mouse lines. DA: dopamine, DAC: dopaminergic amacrine cell, MKO: animals lacking melanopsin phototransduction, RKO: animals lacking rod signaling, CKO: animals lacking cone signaling, DTA: animals where ipRGCs are ablated through expression of diphtheria toxin. Scale bar in (G) is 50 μm. *p < 0.05, bars on plots represent mean.
    2018
    unknown
  11. 2019
    unknown
  12. 2019
    unknown
  13. Figure 2. Quorum sensing controls rapid, VpsL-independent aggregation of V. cholerae in liquid. ; Aggregate formation of the LCD QS-locked (LCD-locked) (A), HCD QS-locked (HCD-locked) (B), and wild-type (WT) (C) V. cholerae strains after 22 h of growth. Shown are representative cross-sections through samples (A–C). The approximate extents of individual aggregates are indicated with white outlines. Magnification: 63X; scale bar: 50 μM. (D) Quantitation of total volume fraction, the total volume of the imaged region that is occupied by aggregates (Materials and methods) within the imaged region for ΔvpsL LCD-locked, ΔvpsL HCD-locked, and ΔvpsL WT strains after 22 h of growth. Representative cross-sections through the ΔvpsL LCD-locked (E–H), ΔvpsL HCD-locked (I–L), and ΔvpsL WT (M–P) V. cholerae strains at 16, 19, 22, and 25 h. (E–P) Magnification: 10X; scale bar: 250 μm. (Q) Quantitation of aggregate volume fraction. The data for T = 22 h are the same as those shown in Figure 2D. Triangle: ΔvpsL LCD-locked, circle: ΔvpsL HCD-locked, and diamond: ΔvpsL WT. (R) Average cluster volume over time for the ΔvpsL HCD-locked (circle) and ΔvpsL WT (diamond) strains. (D,Q,R) Quantitation of mean ± standard deviation (SD; N=3 biological replicates). Mean and SD were calculated using the untransformed data, not the log-transformed data, which results in asymmetric error bars. All strains in all panels harbor the fluorescent mKO reporter constitutively expressed from the chromosome.
    2019
    unknown
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