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ABSTRACT By entering a reversible state of reduced metabolic activity, dormant microorganisms are able to tolerate suboptimal conditions that would otherwise reduce their fitness. Dormancy may also benefit bacteria by serving as a refuge from parasitic infections. Here, we focus on dormancy in the Bacillota , where endospore development is transcriptionally regulated by the expression of sigma factors. A disruption of this process could influence the survivorship or reproduction of phages that infect spore-forming hosts with implications for coevolutionary dynamics. We characterized the distribution of sigma factors in over 4,000 genomes of diverse phages capable of infecting hosts that span the bacterial domain. From this, we identified homologs of sporulation-specific sigma factors in phages that infect spore-forming hosts. Unlike sigma factors required for phage reproduction, we provide evidence that sporulation-like sigma factors are nonessential for lytic infection. However, when expressed in the spore-forming Bacillus subtilis , some of these phage-derived sigma factors can activate the bacterial sporulation gene network and lead to a reduction in spore yield. Our findings suggest that the acquisition of host-like transcriptional regulators may allow phages to manipulate a complex and ancient trait in one of the most abundant cell types on Earth. IMPORTANCE As obligate parasites, phages exert strong top-down pressure on host populations with eco-evolutionary implications for community dynamics and ecosystem functioning. The process of phage infection, however, is constrained by bottom-up processes that influence the energetic and nutritional status of susceptible hosts. Many phages have acquired auxiliary genes from bacteria, which can be used to exploit host metabolism with consequences for phage fitness. In this study, we demonstrate that phages infecting spore-forming bacteria carry homologs of sigma factors, which their hosts use to orchestrate gene expression during spore development. By tapping into regulatory gene networks, phages may manipulate the physiology and survival strategies of nongrowing bacteria in ways that influence host-parasite coevolution. 

Isla Santa Cruz is a volcanic island located in the central Galápagos Archipelago. The island’s northern and southern flanks are deformed by E–W-trending normal faults not observed on the younger Galápagos shields, and Santa Cruz lacks the large summit calderas that characterize those structures. To construct a chronology of volcanism and deformation on Santa Cruz, we employ⁴⁰Ar/³⁹Ar geochronology of lavas and³He exposure dating of fault scarps from across the island. The combination of Ar–Ar dating with in situ-produced cosmogenic exposure age data provides a powerful tool to evaluate fault chronologies. The⁴⁰Ar/³⁹Ar ages indicate that the island has been volcanically active since at least 1.62 ± 0.030 Ma (2SD). Volcanism deposited lavas over the entire island until ~ 200 ka, when it became focused along an E–W-trending summit vent system; all dated lavas < 200 ka were emplaced on the southern flank. Structural observations suggest that the island has experienced two major faulting episodes. Crosscutting relationships of lavas indicate that north flank faults formed after 1.16 ± 0.070 Ma, but likely before 416 ± 36 ka, whereas the faults on the southern flank of the island initiated between 201 ± 37 and 32.6 ± 4.6 ka, based on³He exposure dating of fault surfaces. The data are consistent with a model wherein the northeastern faults are associated with regional extension owing to the young volcano’s location closer to the Galápagos Spreading Center at the time. The second phase of volcanism is contemporaneous with the formation of the southern faults. The expression of this younger, low-volume volcanic phase was likely related to the elongate island morphology established during earlier deformation. The complex feedback between tectonic and volcanic processes responsible for southward spreading along the southern flank likely generated persistent E-W-oriented magmatic intrusions. The formation of the Galápagos Transform Fault and sea-level fluctuations may be the primary causes of eruptive and deformational episodes on Santa Cruz.

 

A morphological dichotomy exists between the active western and older (>1–2.5 Ma) eastern volcanoes of the Galápagos Archipelago. All of the young shield volcanoes in the west have calderas, but none are present on the older volcanoes in the east. This striking difference suggests that there has been a change in volcanic construction and magmatic supply processes, a finding dissimilar to the prevailing Hawaiian model of hot spot evolution. Bouguer anomaly highs (30–50 mGal) consistent with dense cumulate bodies are measured over these calderas. In contrast, we present new gravity data from Santa Cruz and San Cristóbal islands that lack comparable gravity highs. We propose that formation of shallow magma reservoirs and their associated Bouguer anomaly highs were inhibited during evolution of the eastern volcanoes because the proximal Galápagos Spreading Center diverted plume material more efficiently ~1–2 Ma when the spreading center was ~100 km closer to the plume. The difference in caldera expression between the western and eastern islands may be a surface expression of this process. These results suggest that plume‐ridge interaction may play a first‐order role in the evolution of magmatic plumbing systems of near‐ridge ocean islands, which account for one third of hot spot systems.