Mechanical Restoration of California Mixed‐Conifer Forests: Does it Matter Which Trees Are Cut?

The montane ecosystems of northern California have been subjected to repeated manipulation and active fire suppression for over a century, resulting in changes in community structure that contribute to increased wildfire hazard. Ecosystem restoration via reduction of stand density for wildfire hazard mitigation has received substantial attention in recent years; however, many ecological questions remain unanswered. This study compares belowground effects of two alternative forest thinning treatments designed to restore the large, old tree component of late‐seral structure, one of which focuses on restoring Pinus ponderosa dominance (Pine‐preference) and the other of which promotes development of large trees regardless of species (Size‐preference). We evaluated forest floor and soil chemical and microbial parameters in six experimental thinning treatment units of 40 ha each in the Klamath National Forest of northern California 5–6 years after thinning. Inorganic N availability, soil organic C content, phenol oxidase activity, and forest floor C:N ratio were greater in the Size‐preference treatment, whereas forest floor N and soil pH were greater in the Pine‐preference treatment. Our results indicate that these two thinning strategies produce differences in the soil environment that has the potential to affect growth rates of trees that remain, as well as the growth and survivorship of newly established seedlings. Thus, which species/individuals are removed during structural restoration of these mixed‐conifer forests matters both to the belowground components of the ecosystem today and the vegetation and productivity of the ecosystem in future decades.     

Deceived,but not betrayed: static allometry suggests female ornaments in the long-tailed dance fly (Rhamphomyia longicauda) exaggerate condition to males

Evolutionary Ecology - Despite their prevalence in nature, the evolution of sex-specific female ornaments is still not well understood. Although in some cases (often carotenoid-based ornaments)...     

Characterization of Brucella abortus S19 as a challenge strain for use in a mouse model of brucellosis

The objective of this project was to conduct a feasibility study to determine whether the Brucella abortus S19 vaccine infects and persists in mice and determine whether S19 can be used as a challenge strain for vaccine trial studies. Groups of BALB/c mice were inoculated (intraperitoneally, subcutaneously, intranasally) and euthanized to determine colonization titers in the spleens and lungs. This study showed that S19 does infect and persist in the tissues of mice for 8 weeks and demonstrates that S19 can be used, safely and economically under BSL2 containment, as the challenge strain for future trials to evaluate vaccine efficacy.     

Cancer‐secreted miRNAs regulate amino‐acid‐induced mTORC1 signaling and fibroblast protein synthesis

Metabolic reprogramming of non‐cancer cells residing in a tumor microenvironment, as a result of the adaptations to cancer‐derived metabolic and non‐metabolic factors, is an emerging aspect of cancer–host interaction. We show that in normal and cancer‐associated fibroblasts, breast cancer‐secreted extracellular vesicles suppress mTOR signaling upon amino acid stimulation to globally reduce mRNA translation. This is through delivery of cancer‐derived miR‐105 and miR‐204, which target RAGC, a component of Rag GTPases that regulate mTORC1 signaling. Following amino acid starvation and subsequent re‐feeding, ¹³C‐arginine labeling of de novo synthesized proteins shows selective translation of proteins that cluster to specific cellular functional pathways. The repertoire of these newly synthesized proteins is altered in fibroblasts treated with cancer‐derived extracellular vesicles, in addition to the overall suppressed protein synthesis. In human breast tumors, RAGC protein levels are inversely correlated with miR‐105 in the stroma. Our results suggest that through educating fibroblasts to reduce and re‐prioritize mRNA translation, cancer cells rewire the metabolic fluxes of amino acid pool and dynamically regulate stroma‐produced proteins during periodic nutrient fluctuations.     

Using a bistable animal opsin for switchable and scalable optogenetic inhibition of neurons

There is no consensus on the best inhibitory optogenetic tool. Since Gi/o signalling is a native mechanism of neuronal inhibition, we asked whether Lamprey Parapinopsin (“Lamplight”), a Gi/o‐coupled bistable animal opsin, could be used for optogenetic silencing. We show that short (405 nm) and long (525 nm) wavelength pulses repeatedly switch Lamplight between stable signalling active and inactive states, respectively, and that combining these wavelengths can be used to achieve intermediate levels of activity. These properties can be applied to produce switchable neuronal hyperpolarisation and suppression of spontaneous spike firing in the mouse hypothalamic suprachiasmatic nucleus. Expressing Lamplight in (predominantly) ON bipolar cells can photosensitise retinas following advanced photoreceptor degeneration, with 405 and 525 nm stimuli producing responses of opposite sign in the output neurons of the retina. We conclude that bistable animal opsins can co‐opt endogenous signalling mechanisms to allow optogenetic inhibition that is scalable, sustained and reversible.     

Hsp90‐mediated regulation of DYRK3 couples stress granule disassembly and growth via mTORC1 signaling

Stress granules (SGs) are dynamic condensates associated with protein misfolding diseases. They sequester stalled mRNAs and signaling factors, such as the mTORC1 subunit raptor, suggesting that SGs coordinate cell growth during and after stress. However, the molecular mechanisms linking SG dynamics and signaling remain undefined. We report that the chaperone Hsp90 is required for SG dissolution. Hsp90 binds and stabilizes the dual‐specificity tyrosine‐phosphorylation‐regulated kinase 3 (DYRK3) in the cytosol. Upon Hsp90 inhibition, DYRK3 dissociates from Hsp90 and becomes inactive. Inactive DYRK3 is subjected to two different fates: it either partitions into SGs, where it is protected from irreversible aggregation, or it is degraded. In the presence of Hsp90, DYRK3 is active and promotes SG disassembly, restoring mTORC1 signaling and translation. Thus, Hsp90 links stress adaptation and cell growth by regulating the activity of a key kinase involved in condensate disassembly and translation restoration.