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Biology subjects

Roach, F. D.

Publications and source records attributed to Roach, F. D..

2 recordsLinked to original sources

Minimizing co-growth as a broad predictor of community robustness

Microbial communities rarely remain in a fixed physiological state. Instead, they progress through internal life cycles in which changing metabolites, spatial organization, and physiological states reshape ecological interactions over time. Despite extensive theory on coexistence with fixed interactions, we lack simple quantitative predictors of robustness for communities undergoing repeated growth and dispersal cycles. Here we show that a single quantity, the temporal co-growth of community members, predicts robustness across several models of community maturation, including chemotactic spatial patterning, cross-feeding with toxicity, and a phenomenological many-species model with prescribed growth trajectories. Communities in which different species grow at distinct times persist far longer under stochastic reseeding than communities with overlapping growth, with average community lifetime increasing approximately exponentially as co-growth decreases. Across the systems studied here, diverse mechanisms such as spatial organization, metabolic cascades, and physiological programs promote robustness insofar as they reduce the temporal overlap of rapid growth across species. These results identify co-growth as a common quantitative feature of robust dynamically maturing communities and suggest that minimizing co-growth may provide a broader organizing principle for ecological robustness.

ecology↗

The Transcription Factor Xrp1 is Required for PERK-Mediated Antioxidant Gene Induction in Drosophila

PERK is an endoplasmic reticulum (ER) transmembrane sensor that phosphorylates eIF2 to initiate the Unfolded Protein Response (UPR). eIF2 phosphorylation promotes stress-responsive gene expression most notably through the transcription factor ATF4 that contains a regulatory 5 leader. Possible PERK effectors other than ATF4 remain poorly understood. Here, we report that the bZIP transcription factor Xrp1 is required for ATF4-independent PERK signaling. Cell type-specific gene expression profiling in Drosophila indicated that delta-family glutathione-S-transferases (gstD) are prominently induced by the UPR-activating transgene Rh1G69D. Perk was necessary and sufficient for such gstD induction, but ATF4 was not required. Instead, Perk and other regulators of eIF2 phosphorylation regulated Xrp1 protein levels to induce gstDs. The Xrp1 5 leader has a conserved upstream Open Reading Frame (uORF) analogous to those that regulate ATF4 translation. The gstD-GFP reporter induction required putative Xrp1 binding sites. These results indicate that antioxidant genes are highly induced by a previously unrecognized UPR signaling axis consisting of PERK and Xrp1.

cell biology↗