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Abstract Evolution results from the interaction of stochastic and deterministic processes that create a web of historical contingency, shaping gene content and organismal function. To understand the scope of this interaction, we examine the relative contributions of stochasticity, determinism, and contingency in shaping gene inactivation in 34 lineages of endosymbiotic bacteria,Sodalis, found in parasitic lice,Columbicola, that are independently undergoing genome degeneration. Here we show that the process of genome degeneration in this system is largely deterministic: genes involved in amino acid biosynthesis are lost while those involved in providing B-vitamins to the host are retained. In contrast, many genes encoding redundant functions, including components of the respiratory chain and DNA repair pathways, are subject to stochastic loss, yielding historical contingencies that constrain subsequent losses. Thus, while selection results in functional convergence between symbiont lineages, stochastic mutations initiate distinct evolutionary trajectories, generating diverse gene inventories that lack the functional redundancy typically found in free-living relatives. 

Climate-driven sea-level rise is increasing the frequency of coastal flooding worldwide, exacerbated locally by factors like land subsidence from groundwater and resource extraction. However, a process rarely considered in future sea-level rise scenarios is sudden (over minutes) land subsidence associated with great (>M8) earthquakes, which can exceed 1 m. Along the Washington, Oregon, and northern California coasts, the next great Cascadia subduction zone earthquake could cause up to 2 m of sudden coastal subsidence, dramatically raising sea level, expanding floodplains, and increasing the flood risk to local communities. Here, we quantify the potential expansion of the 1 % floodplain (i.e., the area with an annual flood risk of 1%) under low (~0.5 m), medium (~1 m), and high (~2 m) earthquake-driven subsidence scenarios at 24 Cascadia estuaries. If a great earthquake occurred today, floodplains could expand by 90 km² (low), 160 km² (medium), or 300 km² (high subsidence), more than doubling the flooding exposure of residents, structures, and roads under the high subsidence scenario. By 2100, when climate-driven sea-level rise will compound the hazard, a great earthquake could expand floodplains by 170 km² (low), 240 km² (medium), or 370 km² (high subsidence), more than tripling the flooding exposure of residents, structures, and roads under the high subsidence scenario compared to the 2023 floodplain. Our findings can support decision makers and coastal communities along the Cascadia subduction zone as they prepare for compound hazards from earthquake-cycle and climate-driven sea-level rise, and provide critical insights for tectonically active coastlines globally. 

Climate-driven sea-level rise is increasing the frequency of coastal flooding worldwide, exacerbated locally by factors like land subsidence from groundwater and resource extraction. However, a process rarely considered in future sea-level rise scenarios is sudden (over minutes) land subsidence associated with great (>M8) earthquakes, which can exceed 1 m. Along the Washington, Oregon, and northern California coasts, the next great Cascadia subduction zone earthquake could cause up to 2 m of sudden coastal subsidence, dramatically raising sea level, expanding floodplains, and increasing the flood risk to local communities. Here, we quantify the potential expansion of the 1% floodplain (i.e., the area with an annual flood risk of 1%) under low (~0.5 m), medium (~1 m), and high (~2 m) earthquake-driven subsidence scenarios at 24 Cascadia estuaries. If a great earthquake occurred today, floodplains could expand by 90 km²(low), 160 km²(medium), or 300 km²(high subsidence), more than doubling the flooding exposure of residents, structures, and roads under the high subsidence scenario. By 2100, when climate-driven sea-level rise will compound the hazard, a great earthquake could expand floodplains by 170 km²(low), 240 km²(medium), or 370 km²(high subsidence), more than tripling the flooding exposure of residents, structures, and roads under the high subsidence scenario compared to the 2023 floodplain. Our findings can support decision-makers and coastal communities along the Cascadia subduction zone as they prepare for compound hazards from the earthquake cycle and climate-driven sea-level rise and provide critical insights for tectonically active coastlines globally. 

The hazard from earthquake-generated tsunami waves is not only determined by the earthquake’s magnitude and mechanisms, and distance to the earthquake area, but also by the geomorphology of the nearshore and onshore areas, which can change over time. In coastal hazard assessments, a changing coastal environment is commonly taken into account by increasing the sea-level to projected values (static). However, sea-level changes and other climate-change impacts influence the entire coastal system causing morphological changes near- and onshore (dynamic). We compare the run-up of the same suite of earthquake-generated tsunamis to a barrier island-marsh-lagoon-marsh system for statically adjusted and dynamically adjusted sea level and bathymetry. Sea-level projections from 2000 to 2100 are considered. The dynamical adjustment is based on a morphokinetic model that incorporates sea-level along with other climate-change impacts. We employ Representative Concentration Pathways 2.6 and 8.5 without and with treatment of Antarctic Ice-sheet processes (known as K14 and K17) as different sea-level projections. It is important to note that we do not account for the occurrence probability of the earthquakes. Our results indicate that the tsunami run-up hazard for the dynamic case is approximately three times larger than for the static case. Furthermore, we show that nonlinear and complex responses of the barrier island-marsh-lagoon-marsh system to climate change profoundly impacts the tsunami hazard, and we caution that the tsunami run-up is sensitive to climate-change impacts that are less well-studied than sea-level rise. 

Ataxia-telangiectasia mutated (ATM) is one of the three main apical kinases at the crux of DNA damage response and repair in mammalian cells. ATM activates a cascade of downstream effector proteins to regulate DNA repair and cell cycle checkpoints in response to DNA double-strand breaks. While ATM is predominantly known for its role in DNA damage response and repair, new roles of ATM have recently begun to emerge, such as in regulating oxidative stress or metabolic pathways. Here, we report the surprising discovery that ATM inhibition and deletion lead to reduced expression of the nuclear envelope protein lamin A. Lamins are nuclear intermediate filaments that modulate nuclear shape, structure, and stiffness. Accordingly, inhibition or deletion of ATM resulted in increased nuclear deformability and enhanced cell migration through confined spaces, which requires substantial nuclear deformation. These findings point to a novel connection between ATM and lamin A and may have broad implications for cells with ATM mutations—as found in patients suffering from Ataxia Telangiectasia and many human cancers—which could lead to enhanced cell migration and increased metastatic potential.