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Nielsen, C. J. F.

Publications and source records attributed to Nielsen, C. J. F..

2 recordsLinked to original sources

Conserved N-terminal Regulation of the ACA8 Calcium Pump with Two Calmodulin Binding Sites

The autoinhibited plasma membrane calcium ATPase, ACA8 from A. thaliana has an N-terminal autoinhibitory domain. Calcium-bound calmodulin binding at two sites located at residues 42-62 and 74-96 relieves autoinhibition of ACA8 activity. We investigated N-terminally truncated ACA8 constructs (WT, {Delta}20, {Delta}30, {Delta}35, {Delta}37, {Delta}40, {Delta}74 and {Delta}100) to explore the role of conserved motifs in the N-terminal segment preceding the calmodulin binding sites. Furthermore, we purified WT, {Delta}20- and {Delta}100-ACA8, tested activity in vitro and performed structural studies of purified {Delta}20-ACA8 stabilized in its native form to explore the mechanism of autoinhibition. Through activity studies and a yeast complementation assay, we show that an N-terminal segment between residues 20 and 35, upstream of the calmodulin binding sites, is important for autoinhibition and the activation by calmodulin, and that a conserved Phe32 is essential for autoinhibition. Cryo-EM structure determination at 3.3 [A] resolution of a beryllium fluoride inhibited form shows no autoinhibition, but a low-resolution structure for an E1 state indicates autoinhibitory domain binding consistent with the mutational studies and AlphaFold predicted structures.

biochemistry↗

Activation and inhibition of the C-terminal kinase domain of p90 ribosomal S6 kinases

The p90 ribosomal S6 kinases (RSKs) contain two distinct catalytic kinase domains, the N-terminal and C-terminal kinase domains (NTKD and CTKD, respectively). The activation of CTKD is regulated by phosphorylation by extracellular signal-regulated kinase (ERK1/2) and an autoinhibitory L helix. Through a mutational series in vitro of the RSK CTKDs, we found a complex mechanism lifting autoinhibition that led us to design constitutively active RSK CTKDs. These are based on a phosphomimetic mutation and a C-terminal truncation (e.g. RSK2 T577E D694*) where a high activity in absence of ERK phosphorylation is obtained. Using these constructs, we characterize IC50 values of ATP-competitive inhibitors and provide a setup for determining specificity constants (kinact/Ki) of covalent CTKD inhibitors.

biochemistry↗