Fig. 6.

Proposed model for KrsB function. Chemoattractants trigger transient activation of KrsB by intermolecular autophosphorylation in a heterotrimeric G protein-dependent and PI3K- and TorC2-independent manner. Expression of the phospho-mimetic form (T176E) or WT KrsB, which is constitutively phosphorylated, leads to reduced adhesion. On the other hand, krsB⁻ cells and cells in which KrsB is inactive (KrsB_T176A or KrsB_K52R) have increased adhesion that causes reduced motility and chemotaxis, resulting in a streamer phenotype.