The Evolution of the Profile Paradigm in the History of Pedology and Quaternary Geology: Concepts and Applications

55 p.Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2001.This study proposes a unified profile paradigm through the introduction of the pedo-weathering profile (PWP) concept. The pedo-weathering profile demands a re-examination of the pedological subsolum region; a region that has been studied closely by Quaternary geologists. The PWP subsolum contains a C horizon concept of more precisely defined scope than that traditionally used in pedology. In the traditional sense the interval between the solum and bedrock is designated as the C, whether pedogenically modified or not. In the PWP, the C horizon is limited to the part of the traditional C that is pedogenically altered. That part of the subsolum unaltered by pedogenic processes and not having the hardness of bedrock (R) is redefined here as the D horizon. These subsolum horizons exist worldwide in all terranes where fresh geologic materials are exposed at the earth surface and become modified by pedogenic processes; they are the evidence for land surfaces throughout the geologic record. The PWP concept should be useful in disciplines that, in reality, have overlapping interests with pedology.U of I OnlyRestricted to the U of I community idenfinitely during batch ingest of legacy ETD

The Evolution of the Profile Paradigm in the History of Pedology and Quaternary Geology: Concepts and Applications

55 p.Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2001.This study proposes a unified profile paradigm through the introduction of the pedo-weathering profile (PWP) concept. The pedo-weathering profile demands a re-examination of the pedological subsolum region; a region that has been studied closely by Quaternary geologists. The PWP subsolum contains a C horizon concept of more precisely defined scope than that traditionally used in pedology. In the traditional sense the interval between the solum and bedrock is designated as the C, whether pedogenically modified or not. In the PWP, the C horizon is limited to the part of the traditional C that is pedogenically altered. That part of the subsolum unaltered by pedogenic processes and not having the hardness of bedrock (R) is redefined here as the D horizon. These subsolum horizons exist worldwide in all terranes where fresh geologic materials are exposed at the earth surface and become modified by pedogenic processes; they are the evidence for land surfaces throughout the geologic record. The PWP concept should be useful in disciplines that, in reality, have overlapping interests with pedology.U of I OnlyRestricted to the U of I community idenfinitely during batch ingest of legacy ETD

The JNK pathway plays a role in the regulation of mitochondrial transport <i>in vivo</i>.

<p>(A) Representative kymographs of mitochondrial transport with overexpression of JNK kinase (Hep^B2) or knockdown of JNK (Bsk RNAi) in response to paraquat. Anterograde transport is toward the right; retrograde transport is toward the left. (B) Paraquat and/or overexpression of Hep^B2 produce a decrease in mitochondrial flux anterogradly. Knockdown of Bsk partially rescues the effect of paraquat. Both overexpression of Hep^B2 and knockdown of Bsk reduce retrograde flux. (C) Anterograde velocity is reduced by paraquat or overexpression of Hep^B2, while retrograde velocity is reduced in both overexpression of Hep^B2 and knockdown of Bsk. (D) Paraquat treatment shows slightly reduction in retrograde duty cycle with a decrease of moving time; Knockdown of Bsk in response to paraquat shows a slightly increase of pause and a decrease of moving time. (E) Retrograde run length is modestly reduced by paraquat treatment. Either overexpression of Hep^B2 of knockdown of Bsk does not show significant difference compared to controls. (F) Paraquat treatment shows an increase of the percentage of stationary mitochondria, while neither overexpression of Hep^B2 nor knockdown of Bsk shows any difference. The number of larvae analyzed is shown on the bars. Error bars indicate mean ± SEM. Significance is determined by one-way ANOVA with Bonferroni’s post-test. *p<0.05, **p < 0.01, and ***p < 0.001.</p

Ca²⁺ homeostasis is required for normal mitochondrial transport.

<p>(A) Representative Ca²⁺ imaging with H₂O₂ or EGTA/BAPTA treatment is measured by the intensity of GCaMP6 indicator. Scale bars indicate 10 μm. (B) Quantitative results from (A). Ca²⁺ levels are increased by H₂O₂ but reduced with EGTA/BAPTA treatment. (C) Representative kymographs of mitochondrial transport with H₂O₂ or EGTA/BAPTA treatment. Anterograde transport is toward the right; retrograde transport is toward the left. (D) EGTA/BAPTA treatment produces a decrease of mitochondrial transport. The reduced percentage of moving mitochondria by H₂O₂ is further reduced by EGTA/BAPTA treatment. The number of cells analyzed is shown on the bars. Significance is determined by one-way ANOVA with Bonferroni’s post-test. **p < 0.01, and ***p < 0.001.</p

The JNK pathway plays a role in the regulation of mitochondrial transport <i>in vivo</i>.

<p>(A) Representative kymographs of mitochondrial transport with overexpression of JNK kinase (Hep^B2) or knockdown of JNK (Bsk RNAi) in response to paraquat. Anterograde transport is toward the right; retrograde transport is toward the left. (B) Paraquat and/or overexpression of Hep^B2 produce a decrease in mitochondrial flux anterogradly. Knockdown of Bsk partially rescues the effect of paraquat. Both overexpression of Hep^B2 and knockdown of Bsk reduce retrograde flux. (C) Anterograde velocity is reduced by paraquat or overexpression of Hep^B2, while retrograde velocity is reduced in both overexpression of Hep^B2 and knockdown of Bsk. (D) Paraquat treatment shows slightly reduction in retrograde duty cycle with a decrease of moving time; Knockdown of Bsk in response to paraquat shows a slightly increase of pause and a decrease of moving time. (E) Retrograde run length is modestly reduced by paraquat treatment. Either overexpression of Hep^B2 of knockdown of Bsk does not show significant difference compared to controls. (F) Paraquat treatment shows an increase of the percentage of stationary mitochondria, while neither overexpression of Hep^B2 nor knockdown of Bsk shows any difference. The number of larvae analyzed is shown on the bars. Error bars indicate mean ± SEM. Significance is determined by one-way ANOVA with Bonferroni’s post-test. *p<0.05, **p < 0.01, and ***p < 0.001.</p

ROS changes mitochondrial motility mainly by reducing flux and velocity <i>in vivo</i>.

<p>(A) Representative kymographs of mitochondrial transport under paraquat treatment. Anterograde transport is toward the right; retrograde transport is toward the left. (B) Paraquat treatment produces a decrease in mitochondrial flux, which is rescued by overexpression of SOD1 or SOD2 in both directions. (C) Velocity is reduced with paraquat treatment, and this is rescued by SOD1 or SOD2 overexpression in both directions. (D) Paraquat treatment shows a small reduction in retrograde duty cycle with an increase of pause time and a decrease of moving time; overexpression of SOD1 shows a small increase of pause time. (E) Retrograde run length is modestly reduced with paraquat treatment. (F) Paraquat treatment shows an increase of the percentage of stationary mitochondria, which is rescued by SOD overexpression. The percentage of anterograde moving mitochondria increases with SOD2 overexpression. (G) Mitochondrial density is comparable to control with paraquat treatment or SOD overexpression. The number of larvae analyzed is shown on the bars. Error bars indicate mean ± SEM. Significance is determined by one-way ANOVA with Bonferroni’s post-test. *p<0.05, **p < 0.01, and ***p < 0.001.</p

ROS regulation of axonal mitochondrial transport is mediated by Ca²⁺ and JNK in <i>Drosophila</i>

<div><p>Mitochondria perform critical functions including aerobic ATP production and calcium (Ca²⁺) homeostasis, but are also a major source of reactive oxygen species (ROS) production. To maintain cellular function and survival in neurons, mitochondria are transported along axons, and accumulate in regions with high demand for their functions. Oxidative stress and abnormal mitochondrial axonal transport are associated with neurodegenerative disorders. However, we know little about the connection between these two. Using the <i>Drosophila</i> third instar larval nervous system as the <i>in vivo</i> model, we found that ROS inhibited mitochondrial axonal transport more specifically, primarily due to reduced flux and velocity, but did not affect transport of other organelles. To understand the mechanisms underlying these effects, we examined Ca²⁺ levels and the JNK (c-Jun N-terminal Kinase) pathway, which have been shown to regulate mitochondrial transport and general fast axonal transport, respectively. We found that elevated ROS increased Ca²⁺ levels, and that experimental reduction of Ca²⁺ to physiological levels rescued ROS-induced defects in mitochondrial transport in primary neuron cell cultures. In addition, <i>in vivo</i> activation of the JNK pathway reduced mitochondrial flux and velocities, while JNK knockdown partially rescued ROS-induced defects in the anterograde direction. We conclude that ROS have the capacity to regulate mitochondrial traffic, and that Ca²⁺ and JNK signaling play roles in mediating these effects. In addition to transport defects, ROS produces imbalances in mitochondrial fission-fusion and metabolic state, indicating that mitochondrial transport, fission-fusion steady state, and metabolic state are closely interrelated in the response to ROS.</p></div

The percentage of moving mitochondria is reduced in response to ROS and rescued by SOD overexpression <i>in vitro</i>.

<p>(A) Representative kymographs of mitochondrial transport under H₂O₂ treatment. Anterograde transport is toward the right; retrograde transport is toward the left. (B) The percentage of moving mitochondria is reduced with H₂O₂ treatment. SOD1 or SOD2 overexpression can rescue the defect. The number of cells analyzed is shown on the bars. Error bars indicate mean ± SEM. Significance is determined by one-way ANOVA with Bonferroni’s post-test. *p<0.05 and ***p < 0.001.</p

Mitochondrial length, membrane potential, and transport are interrelated in response to ROS.

<p>(A) Representative images of mitochondrial length and membrane potential. Mitochondrial lengths are measured using mitoGFP signals and mitochondrial membrane potential is measured using TMRM staining by the intensity ratio of mitochondrial fluorescence to cytosolic fluorescence. Scale bars indicate 10 μm. (B) Quantitative results of mitochondrial length. ROS treatment shows a decrease of mitochondrial length, which is rescued by SOD1 or SOD2 overexpression. (C) Quantitative results of mitochondrial membrane potential. Mitochondrial membrane potential is reduced under oxidative stress conditions. SOD1 or SOD2 overexpression does not rescue these defects. (D) Representative images of mitochondrial length measured using the mitoGFP signal. Scale bars indicate 10 μm. (E) H₂O₂ and/or EGTA/BAPTA reduce mitochondrial length, which is consistent with the results of mitochondrial transport (Figs <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0178105#pone.0178105.g004" target="_blank">4K, 4L</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0178105#pone.0178105.g005" target="_blank">5C and 5D</a>). The number of cells analyzed is shown on the bars. Error bars indicate mean ± SEM. Significance is determined by one-way ANOVA with Bonferroni’s post-test. *p<0.05, **p < 0.01, and ***p < 0.001.</p