Author Correction: Identifying threshold responses of Australian dryland rivers to future hydroclimatic change.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Identifying threshold responses of Australian dryland rivers to future hydroclimatic change.

Rivers provide crucial ecosystem services in water-stressed drylands. Australian dryland rivers are geomorphologically diverse, ranging from through-going, single channels to discontinuous, multi-channelled systems, yet we have limited understanding of their sensitivity to future hydroclimatic changes. Here, we characterise for the first time the geomorphology of 29 dryland rivers with catchments across a humid to arid gradient covering >1,800,000 km2 of continental eastern and central Australia. Statistical separation of five specific dominantly alluvial river types and quantification of their present-day catchment hydroclimates enables identification of potential thresholds of change. Projected aridity increases across eastern Australia by 2070 (RCP4.5) will result in ~80% of the dryland rivers crossing a threshold from one type to another, manifesting in major geomorphological changes. Dramatic cases will see currently through-going rivers (e.g. Murrumbidgee, Macintyre) experience step changes towards greater discontinuity, characterised by pronounced downstream declines in channel size and local termination. Expanding our approach to include other river styles (e.g. mixed bedrock-alluvial) would allow similar analyses of dryland rivers globally where hydroclimate is an important driver of change. Early identification of dryland river responses to future hydroclimatic change has far-reaching implications for the ~2 billion people that live in drylands and rely on riverine ecosystem services.

RIPK1- and RIPK3-induced cell death mode is determined by target availability.

Both receptor-interacting protein kinase 1 (RIPK1) and RIPK3 can signal cell death following death receptor ligation. To study the requirements for RIPK-triggered cell death in the absence of death receptor signaling, we engineered inducible versions of RIPK1 and RIPK3 that can be activated by dimerization with the antibiotic coumermycin. In the absence of TNF or other death ligands, expression and dimerization of RIPK1 was sufficient to cause cell death by caspase- or RIPK3-dependent mechanisms. Dimerized RIPK3 induced cell death by an MLKL-dependent mechanism but, surprisingly, also induced death mediated by FADD, caspase 8 and RIPK1. Catalytically active RIPK3 kinase domains were essential for MLKL-dependent but not for caspase 8-dependent death. When RIPK1 or RIPK3 proteins were dimerized, the mode of cell death was determined by the availability of downstream molecules such as FADD, caspase 8 and MLKL. These observations imply that rather than a 'switch' operating between the two modes of cell death, the final mechanism depends on levels of the respective signaling and effector proteins.