FIGURE 10.

Schematic distribution of CK and compartmentation of CK metabolism in Arabidosis. CK biosynthesis was localized mainly to plastids and further to mitochondrion and cytosol (Kasahara et al., 2004) followed by their activation that occurs within cytosol (Chen and Kristopeit, 1981a,b; Kuroha et al., 2009). Distribution of distinct CK forms within cellular compartments was elucidated in our recent publication (Jiskrová et al., 2016). Almost no active CK content in apoplast in comparison to CK glucosides is given by the fact that CK degradation takes place prevalently there (Werner et al., 2003). Besides CK degradation in apoplast, two of its enzymes were localized in vacuoles (Werner et al., 2003), whereas only one enzyme (CKX7) was revealed to play its role in cytoplasm (Köllmer et al., 2014). In this study, we confirmed localization of CK glucosylation in cytosol, thereby suggesting a transport mechanism of CK glucosides across plasma membrane out of the cytosol. The only known transporters of CK up to date are purine permeases (PUP) transporting iP and tZ (Gillissen et al., 2000; Bürkle et al., 2003; Cedzich et al., 2008), and equilibrative nucleoside transporters (ENT) (Sun et al., 2005; Hirose et al., 2007). Perception and signal transduction of CK was described in many works up to now (for review, see Kakimoto, 2003; or Spíchal, 2012). In this scheme, we adopt a hypothesis from our review (Zalabák et al., 2013) where recycling of AHK monomers between endosomes and plasma membrane (Dortay et al., 2008; Lomin et al., 2011) is proposed as a possible compromise scenario.