Integrin-linked kinase

ILK1 is linked to hyperosmotic stress sensitivity.[23] ILK1 reduced salt stress in seedlings placed in solution with increased concentrations of salt.[10] ILK1 concentrations remain fairly constant throughout development regardless of a high salt exposure.[23] Previously, it was believed that K⁺ accumulation was reduced in increased salt concentration.[24] K⁺ homeostasis is not affected in high salt concentrations. During periods of high salt stress, K⁺ concentrations in the presence of ILK1 was maintained at the existing level. Potassium transport is required for flg22 root growth inhibition and potassium transport was affected by flg22.[23]

Potassium levels modulate the activation of flg22, a flagellin peptide composed of 22 amino acids that triggers pathogen-associated molecular patterns (PAMPs). PAMPs functions by activating regulators of bacterial pathogen alert system.[23][25] Ion concentration levels of Mn²⁺, Mg²⁺, S and Ca²⁺ were also affected after PAMP regulators were mobilized.[23]

Potassium (K⁺) is responsible for osmoregulation, membrane potential maintenance and turgor pressure of plant cells which in turn mediates stomata movement and growth of tubules within the plant.[26] Photosynthesis and other metabolic pathways are controlled by potassium.[26] When sufficient K⁺ uptake is not met, PAMPs are activated. Calmodulins, specifically CML9, have appeared as important genes to interact with ILK1 and regulate potassium levels within the cell. While CLM9 primarily regulates Ca²⁺ it is linked to a yet identified K⁺/Ca²⁺ influx channel.[10] While interactions are known to occur between CML9 and ILK1, ILK1 Is not a direct phosphorylation target of CML9. With the addition of CML9, autophosphorylation of ILK1 is diminished, the present irrespective of calcium available for uptake.

A) Full length protein sequence of Arabidopsis. B) 3D structures of ILK repeats. C) N-terminal is blue C-terminal is red. Shows the succession of secondary elements. D) Amino acid sequence of ILK.

ILK1 is also affected by presence or absence of manganese (Mn²⁺). Autophosphorylation and substrate phosphorylation occurred when exposed to both Mn²⁺ and Mg^2+. Mn²⁺ and was dose dependent where Mg²⁺ was not. Specific ILK autophosphorylation sites were found in the presence of Mn²⁺ but not in the presence of Mg²⁺ which supports the ILK1 dependent phosphorylation suggested above.[10] Mass spectrometry revealed no other kinases were present to trigger this response.

ILK1 has been found to promote resistance in bacterial pathogens.[10] ILK1 is required for flg22 sensitivity in seedlings. A catalytically inactive version of ILK1 was compared with catalytically active versions of ILK1 to see the level of resistance when challenged with bacterial pathogens. Plants inoculated with inactive ILK1 were more susceptible to bacterial infection than active ILK1 suggesting that ILK1 is needed for bacterial pathogen detection. While ILK1 is involved in bacterial pathogen detection it is not used for effect induced defenses.[23]

ILK1 increases PAMP response and basal immunity through phosphorylation of MPK3 and MPK6 and operates independently in reactive oxygen species (ROS) production. High Affinity Potassium uptake mediators such as HAK5 have also been found to be integral in the signaling of flg22.[23] HAK5 function when potassium levels are low.[23] Flg22 has been shown to depolarize the cell's plasma membrane with HAK5 and ILK1 working together to mediate ion homeostasis to assist with both short and long term actions such as growth and suppression thereof.[23]