Back

Kidney-Specific WNK1 Amplifies NCC Responsiveness to Potassium Imbalance

Boyd-Shiwarski, C. R.; Beacham, R. T.; Griffiths, S. E.; Shiwarski, D. J.; Knoell, S. A.; Nkashama, L. J.; Querry, K. E.; Marciszyn, A. L.; Huang, C.-L.; Stocker, S. D.; Subramanya, A. R.

2021-03-12 physiology
10.1101/2021.03.12.435046 bioRxiv
Show abstract

To maintain potassium homeostasis, the kidneys distal convoluted tubule (DCT) converts small changes in blood [K+] into robust effects on salt reabsorption. This process requires NaCl cotransporter (NCC) activation by WNK kinases. During hypokalemia, the Kidney-Specific WNK1 isoform (KS-WNK1) scaffolds the DCT-expressed WNK signaling pathway within biomolecular condensates of unknown function termed WNK bodies. Here, we show that KS-WNK1 amplifies the dynamic range of NCC activity in response to potassium imbalance, in part via WNK bodies. Targeted condensate disruption traps the WNK pathway, causing renal salt-wasting that is more pronounced in females. In humans, WNK bodies accumulate as plasma potassium falls below 4.0mmol/L, suggesting avid condensate-mediated salt reabsorption even when [K+] is low-normal. These data identify WNK bodies as signal amplifiers that mediate tubular potassium responsiveness, nephron sexual dimorphism, and blood pressure salt-sensitivity. Our results illustrate how condensate specialization can optimize a mammalian physiologic stress response that impacts human health.

Matching journals

The top 7 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.