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Depew, C.

Publications and source records attributed to Depew, C..

2 recordsLinked to original sources

Cover crop microbiomes affect legume cash crop growth but not consistently through enriching nitrogen-fixing rhizobia

Harnessing plant-microbe interactions offers a promising path to reduce chemical inputs and enhance crop resilience in agricultural systems. However, microbial inoculants often fail to persist or function consistently across soils, which limits their broad utility. Here, we explore whether legume cover crops can be used to create microbial legacies that improve nodulation and nitrogen fixation in downstream legume cash crops. In a greenhouse experiment, we inoculated four cash crops with rhizosphere and nodule microbiomes derived from different legume cover crops, then used 16S rRNA and nifH amplicon sequencing to profile bacterial and diazotroph communities, respectively. Host identity shaped cover crop rhizosphere and nodule microbial communities, and specific taxa within these communities predicted nodulation and growth in some cash crops. Host specificity varied widely across cash crops, with alfalfa narrowly dependent on a specific symbiont and common bean and fava bean forming more permissive, taxonomically diverse nodule communities. Increased nodulation did not consistently improve biomass, and outcomes in some cash crops depended on more than symbiont compatibility alone. In particular, common bean growth was predicted by both rhizobial and non-rhizobial taxa, while soybean nodulation was shaped by its compatible symbiont as well as a mismatched rhizobial taxon associated with other hosts. Together, these results suggest that cover crops can shape cash crop microbiomes and productivity in host-specific ways, requiring precise symbiont matching in selective hosts but offering more flexible, multi-taxon management opportunities in permissive hosts.

plant biology↗

Effect of altered production and storage of dopamine on development and behavior in C. elegans

The nematode, Caenorhabditis elegans, is an advantageous model for studying developmental toxicology due to its homology to humans and well-defined developmental stages. Similarly to humans, C. elegans utilize dopamine as a neurotransmitter to regulate motor behavior. We have previously reported behavioral deficits in a genetic model of C. elegans (OK411) that lack the neurotransmitter transporter necessary for packaging dopamine into synaptic vesicles. Anecdotally, we observed these C. elegans appeared to have a smaller body size, which is supported by prior studies that observed a larger body size in C. elegans that lack the enzyme that catalyzes dopamine synthesis, suggesting a complex regulatory system in which dopamine mediates body size in C. elegans. However, the question of whether body size abnormalities apparent in C. elegans with disruptions to their dopamine system are developmental or purely based on body size remains unanswered. Here, we present data characterizing the effect of gene mutations in dopamine-related proteins on body size, development, and behavior. We analyzed C. elegans that lack the ability to sequester dopamine (OK411), that overproduce dopamine (UA57), and a novel strain (MBIA) generated through crossing OK411 and UA57, which lacks the ability to sequester dopamine into vesicles and additionally endogenously overproduces dopamine. This novel strain was generated to address the hypothesis that an endogenous increase in production of dopamine can rescue deficits caused by a lack of vesicular dopamine sequestration. Compared to wild type, OK411 have shorter body lengths and behavioral deficits in early life stages. In contrast, the MBIA strain have similar body lengths to wild-type by early adulthood and display similar behavior to wild-type by early adulthood. Our data suggests that endogenously increasing the production of dopamine is able to mitigate deficits in C. elegans lacking the ability to package dopamine into synaptic vesicles. These results provide evidence that the dopamine system impacts development, growth, and reproduction in C. elegans.

neuroscience↗