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To balance the flux of sulfur (S) into glucosinolates (GSL) and primary metabolites plants exploit various regulatory mechanisms particularly important upon S deficiency (−S). The role of MYB34, MYB51 and MYB122 controlling the production of indolic glucosinolates (IGs) and MYB28, MYB29, and MYB76 regulating the biosynthesis of aliphatic glucosinolates (AGs) in  Arabidopsis thaliana  has not been fully addressed at −S conditions yet. We show that the decline in the concentrations of GSL during S depletion does not coincide with the globally decreased transcription of  R2R3-MYBs . Whereas the levels of GSL are diminished, the expression of  MYB34, MYB51, MYB122 , and  MYB28  is hardly changed in early phase of S limitation. Furthermore, the mRNA levels of these  MYBs  start to raise under prolonged S starvation. In parallel, we found that SLIM1 can downregulate the  MYBs in vitro  as demonstrated in  trans -activation assays in cultured  Arabidopsis  cells with  SLIM1  as effector and  ProMYB51:uidA  as a reporter construct. However,  in vivo , only the mRNA of  MYB29  and  MYB76  correlated with the levels of GSL at −S. We propose that the negative effect of SLIM1 on GSL regulatory genes can be overridden by a “low GSL signal” inducing the transcription of  MYBs  in a feedback regulatory loop. In accordance with this hypothesis, the expression of  MYB34, MYB51, MYB122 , and  CYP83B1  was further induced in  cyp79b2 cyp79b3  mutant exposed to −S conditions vs.  cyp79b2 cyp79b3  plants grown on control medium. In addition, the possible role of  MYBs  in the regulation of essential S assimilation enzymes, in the regulation of GSL biosynthesis upon accelerated termination of life cycles, in the mobilization of auxin and lateral root formation at S deficiency is discussed.

Update on the role of R2R3-MYBs in the regulation of glucosinolates upon sulfur deficiency