About Me.

Investigating the relationship between environmental factors and nutrition in returning Pacific salmon spawners. Fish used in study are sourced nearly exclusively from Indigenous hatcheries and Indigenous owned/run businesses

Updates to come!

Organizing a public outreach cultural event. Wild-caught Pacific salmon sourced from regional Indigenous-owned/run businesses will be prepared and served to attendees while informational talks are given regarding the importance of fostering salmon population persistence for future generations.

Event date: April 29th, 2023

Event location: Reaney Park, Pullman, WA

Visit the event website for more info:

https://mphelpslab.org/hope-for-salmon

Mitochondria-mediated Maternal-fetal Interactions and Consequences of Mitochondrial Dysregulation Indicate New Roles for Mitochondria in Hypertensive Pregnancies

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Oxidative stress, placental mitochondrial morphological alterations, and impaired bioenergetics are associated with hypertensive disorders of pregnancy. Here we examined mitochondrial DNA mutational load in pregnant women with pregnancy-induced hypertension and reanalyzed publicly available high-throughput transcriptomic datasets from maternal and fetal tissues from normotensive and hypertensive pregnancies. Mitochondrial dysregulation was indicated by aberrant mitochondrial gene expression, and putative consequences were examined. Women with hypertensive pregnancy had elevated mitochondrial DNA mutational load. Maternal mitochondrial dysregulation in hypertensive pregnancies was associated with pathways involved in inflammation, cell death/survival, and placental development. In fetal tissues from hypertensive pregnancies, mitochondrial dysregulation was associated with increased extracellular vesicle production. Our study demonstrates mitochondria-mediated maternal-fetal interactions during healthy pregnancy and maternal mitochondrial dysregulation in hypertensive pregnancy development.

Reduced Maternal Circulating Cell-Free Mitochondrial DNA Is Associated With the Development of Preeclampsia

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Abstract

Background Circulating cell-free mitochondrial DNA (ccf-mtDNA) is a damage-associated molecular pattern that reflects cell stress responses and tissue damage, but little is known about ccf-mtDNA in preeclampsia. The main objectives of this study were to determine (1) absolute concentrations of ccf-mtDNA in plasma and mitochondrial DNA content in peripheral blood mononuclear cells and (2) forms of ccf-mtDNA transport in blood from women with preeclampsia and healthy controls. In addition, we sought to establish the association between aberrance in circulating DNA-related metrics, including ccf-mtDNA and DNA clearance mechanisms, and the clinical diagnosis of preeclampsia using bootstrapped penalized logistic regression. Methods and Results Absolute concentrations of ccf-mtDNA were reduced in plasma from women with preeclampsia compared with healthy controls (P≤0.02), while mtDNA copy number in peripheral blood mononuclear cells did not differ between groups (P>0.05). While the pattern of reduced ccf-mtDNA in patients with preeclampsia remained, DNA isolation from plasma using membrane lysis buffer resulted in 1000-fold higher ccf-mtDNA concentrations in the preeclampsia group (P=0.0014) and 430-fold higher ccf-mtDNA concentrations in the control group (P<0.0001). Plasma from women with preeclampsia did not induce greater Toll-like receptor-9-induced nuclear factor kappa-light-chain enhancer of activated B cells-dependent responses in human embryonic kidney 293 cells overexpressing the human TLR-9 gene (P>0.05). Penalized regression analysis showed that women with preeclampsia were more likely to have lower concentrations of ccf-mtDNA as well as higher concentrations of nuclear DNA and DNase I compared with their matched controls. Conclusions Women with preeclampsia have aberrant circulating DNA dynamics, including reduced ccf-mtDNA concentrations and DNA clearance mechanisms, compared with gestational age-matched healthy pregnant women.

The cell-surface protein composition of a coral symbiont, Breviolum psygmophilum, reveals a mechanism for host specificity and displays dynamic regulation during temperature stress

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Abstract

The symbiosis between corals and dinoflagellates in the family Symbiodiniaceae is threatened by warming trends that induce coral bleaching, or symbiosis breakdown. Current models of symbiosis breakdown involve an immune response to an elevation in reactive oxygen species that ultimately results in the loss of the symbiont. However, the intimate nature of the symbiosis implies an important role for the symbiont surface as a point of interaction between partners. The response of symbiont cell surface proteins to experimental temperature stress was, therefore, investigated using a cell surface biotin probe. Cell-surface protein composition was found to be dynamically regulated in response to heat stress, particularly after 24 h of exposure to heat treatment. This pattern was primarily driven by an increased abundance in heat shock proteins, demonstrating that stress experienced by the symbiont can manifest at the cell surface. Elements known to activate host immunity were also increased in response to temperature stress, further demonstrating an avenue by which the symbiont can elicit a host immune response independent of reactive oxygen species. This work documents the cell surface protein composition of a Symbiodiniaceae species for the first time and highlights host–symbiont interaction mechanisms that may be important during symbiosis breakdown.