Primary succession in an Atlantic saltmarsh: from intertidal flats to mid-marsh platform in 35 years

Although salt marsh is a classic example of primary succession, the underlying mechanisms and their time-scales are poorly understood. As salt marsh succession depends on sediment accretion, the amelioration of abiotic conditions associated with increasing elevation suggests potential explanatory roles for facilitation, competition and the stress-gradient hypothesis. We present a 35-year longitudinal study of salt marsh development from intertidal flat to a mid-marsh platform at Odiel Marshes in south-western Iberia. Using permanent plots, this work chronicles changes in elevation and marsh morphology, their evolving effects on sediment redox potential and salinity and the colonisation and changing patterns of dominance of halophytic species. Sporadically colonising clumps of the low-marsh species Spartina maritima trapped sediment to form raised tussocks, which increased in elevation and area. Reduced tidal inundation and locally improved drainage promoted higher redox potentials and allowed colonisation by a sequence of species less tolerant of reducing conditions: Sarcocornia perennis, its hybrid with high-marsh S. fruticosa, and Atriplex portulacoides. Unlike its centrifugally colonising predecessors, A. portulacoides invaded from the tussock edges. Transplant experiments designed to investigate its late establishment on tussocks showed that seedling survival depended on elevational differences as small as 4 cm. After increasing in elevation by c. 1 m (c. 29 mm/year), coalescence of the tussocks formed a marsh platform at a level corresponding to mean high tides. This supports a theoretical punctuated transition from ‘submergence marsh’ to ‘emergence marsh’, previously postulated for this tidal elevation. Synthesis. The unexpected rapidity of this primary succession highlights the central role of facilitation. Vertical sediment accretion, locally engineered by colonising species, progressively alleviates abiotic stress and allows colonisation by species that are less tolerant of chemically reducing conditions but are ultimately better competitors

Functional Interactions between KCNE1 C-Terminus and the KCNQ1 Channel

The KCNE1 gene product (minK protein) associates with the cardiac KvLQT1 potassium channel (encoded by KCNQ1) to create the cardiac slowly activating delayed rectifier, IKs. Mutations throughout both genes are linked to the hereditary cardiac arrhythmias in the Long QT Syndrome (LQTS). KCNE1 exerts its specific regulation of KCNQ1 activation via interactions between membrane-spanning segments of the two proteins. Less detailed attention has been focused on the role of the KCNE1 C-terminus in regulating channel behavior. We analyzed the effects of an LQT5 point mutation (D76N) and the truncation of the entire C-terminus (Δ70) on channel regulation, assembly and interaction. Both mutations significantly shifted voltage dependence of activation in the depolarizing direction and decreased IKs current density. They also accelerated rates of channel deactivation but notably, did not affect activation kinetics. Truncation of the C-terminus reduced the apparent affinity of KCNE1 for KCNQ1, resulting in impaired channel formation and presentation of KCNQ1/KCNE1 complexes to the surface. Complete saturation of KCNQ1 channels with KCNE1-Δ70 could be achieved by relative over-expression of the KCNE subunit. Rate-dependent facilitation of K+ conductance, a key property of IKs that enables action potential shortening at higher heart rates, was defective for both KCNE1 C-terminal mutations, and may contribute to the clinical phenotype of arrhythmias triggered by heart rate elevations during exercise in LQTS mutations. These results support several roles for KCNE1 C-terminus interaction with KCNQ1: regulation of channel assembly, open-state destabilization, and kinetics of channel deactivation