Concerning tissue-specific responses, the coleoptile was the only organ which showed an even response to both Pcz and Ucz treatment in Mo20W, A619, and B73. In Torin 1 contrast, Pcz sensitivity in the roots and true leaves ranged from resistant to highly susceptible. The degree of Pcz response in maize roots seems therefore dependent on the genetic Masitinib clinical trial background of the maize line. The data also indicates differential hormonal regulation of tissue growth in aerial organs of maize inbreds. In rice and wheat tissue culture, accumulation of Pcz against a concentration gradient has been reported. This indicates active uptake systems in these grass species. In Monilinia fructicola, the ABC transporter MfABC1 is induced upon Pcz treatment, which suggests a possible role for transporters of the ABC family in Pcz uptake in plants and fungi. Differences in either root uptake, in planta transport, and/or Pcz catabolism may be responsible for the observed variances between maize inbreds. Nonetheless, our results also indicated a relation of Pcz- and BLsensitivity between the inbred lines. Compared 
to Mo20W and B73, W22 and A619 plants exhibited a smaller inhibition of root elongation in the presence of either Pcz or higher concentrations of BL. We therefore conclude that the genetic diversity between these maize lines influences their response to BRs. Death induced by the intrinsic mitochondrial pathway is initiated by perturbation of the mitochondrial membrane, and proceeds via release of cytochrome c and other apoptogenic factors from the intermembrane space of this organelle. This process is tightly regulated by the anti- and pro-apoptotic members of the Bcl-2 family. Cytochrome c release in response to various types of cellular stress is suggested to occur via pores formed by homo and hetero-oligomers of the pro-apoptotic Bcl-2 family members Bak and Bax. The actual ratio of anti- to proapoptotic Bcl-2 family members constitutes a sensor and sets the threshold of susceptibility to apoptosis for the cell. That the relative abundance of anti-apoptotic and pro-apoptotic regulators also critically influences tumorigenesis is illustrated by the recurring perturbation of this balance in cancer. Consequently, the expression of Bcl-2 family members is normally tightly regulated at multiple levels including transcriptional activation and proteasomal degradation. In recent years, microRNAs have emerged as important regulators of gene expression. MicroRNAs are 21-23 bp long non-coding RNAs that function mainly through targeting the 39UTR of specific genes and thereby inhibiting the translation of their encoded protein or degrading the target mRNA. With their ability to regulate multiple genes simultaneously, microRNAs have fundamental roles in such diverse processes as proliferation, apoptosis and differentiation. Furthermore, many microRNAs, such as those of the miR-15, let-7, or miR-17 families have been shown to be deregulated in cancer, resulting in the altered expression of target genes important for tumor development. Some Bcl-2 family members have been shown to be regulated by microRNAs, such as Bcl-2, which is regulated by miR-15/16 and miR-148a, and Mcl-1, which is regulated by miR-29. However, for many of the Bcl-2 family members, including the pro-apoptotic p53 target gene Noxa, it is unknown whether microRNA regulation takes place. Like other BH3-only proteins, Noxa has the capacity to bind and neutralize pro-survival Bcl-2 family members. However, it has a restricted binding pattern and mainly interacts with Mcl-1. Among other things, this interaction leads to proteasomal degradation of Mcl-1, which in turn has been shown to be a prerequisite for apoptosis in response to for example UV irradiation.