The mechanism(s) of glucose sensing for inducing the autophagic peroxisome degradation (pexophagy) is not known. Recently, we have found that defects in the S. cerevisiae PKA-cAMP signaling pathway due to knockouts of GPR1 and/or GPA2 suppressed glucose-induced degradation of peroxisomal thiolase. Here we report that single defects of high (SNF3) and low (RGT2) affinity glucose sensors involved in glucose-dependent induction of hexose transporters have only a slight effect on glucose-induced degradation of peroxisomal thiolase, although simultaneous defects of both sensors, SNF3 and RGT2 (which are known to strongly affect glucose transport) strongly inhibit this process in S. cerevisiae. Most likely, glucose is sensed for pexophagy using the Gpr1 sensor involved in the PKA-cAMP signaling pathway. In the methylotrophic yeast P. pastoris, however, knock out of S. cerevisiae orthologs of GPR1 and GPA2 did not affect glucose-induced degradation of oleate-induced thiolase or the methanolinduced key peroxisomal protein, alcohol oxidase. This implies that glucose sensing for pexophagy is different in baker's and methylotrophic yeasts.