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Suggests that all members on the household may possibly function as transcription factors, although this has not been functionally demonstrated for all members.Six of your type-B ARRs (ARR11, ARR14, and ARR18 of subfamily 1; ARR13 of subfamily 2; and ARR19 and ARR20 of subfamily 3) were unable to rescue the arr1 arr12 mutant, pointing to functional distinction(s) among the 11 type-B ARRs of Arabidopsis. These similarities and differences probably relate in part towards the potential of the type-B ARRs to transcriptionally regulate an overlapping set of primary-response genes, according to the recognized function of type-B ARRs in transcriptional regulation (Sakai et al., 2000, 2001; Imamura et al., 2001, 2003; Lohrmann et al., 2001; Hosoda et al., 2002; Mason et al., 2004, 2005; Rashotte et al., 2006; Liang et al., 2012; Tsai et al., 2012). DNA-binding studies indicate that ARR11, unlike ARR1, ARR2, and ARR10, doesn’t bind for the core AGATT sequence (Sakai et al., 2000; Hosoda et al., 2002; Imamura et al., 2003; Taniguchi et al., 2007). Similarly, in yeast (Saccharomyces cerevisiae) one-hybrid assays, ARR2 but not ARR11 associates with an anther/ pollen-specific promoter fragment (Lohrmann et al., 2001). These information are consistent with our finding that ARR11 can not functionally substitute for ARR1 or ARR12 and recommend that this arises in aspect from differences in their target specificity. The inability of ARR18 to complement arr1 arr12 also likely arises in component as a result of differences from ARR1 with regards to target affinity or specificity depending on our transcriptional analysis. Whereas transgenic expression of ARR1 in arr1 arr12 facilitated cytokinin-mediated induction with the primary-response genes ARR5 and ARR15 and cytokinin-mediated suppression of HKT1, transgenic expression of ARR18 only facilitated the suppression of HKT1. Also, though we observed that ARR18 functioned as a transcription factor within a transient protoplast expression method, it differed from ARR1 and ARR12 in that it did not activate the ARR6 reporter inside a cytokinin-dependent fashion. Variations within the capacity in the type-B ARRs to transcriptionally regulate targets need to have not just arise from individual differences in target affinity or specificity, but could also arise from differences in type-B ARR protein stability (Kim et al., 2012) or their interactions with upstream regulators like the ARABIDOPSIS HISCONTAINING PHOSPHOTRANSFER PROTEINS and/or transcriptional coregulators (Dortay et al., 2006; Kim et al., 2006). As an example, ARR2 appears to be specifically activated through an AHK3-dependent phosphorelay inside the regulation of leaf senescence (Kim et al., 2006). A possible lack on the relevant regulators would preclude the activation of the type-B ARRs.Fmoc-OSu Technical Information The inability of ARR11, ARR14, ARR18, ARR19, and ARR20 to complement the arr1 arr12 mutant phenotype is not what 1 would necessarily predict according to prior characterization applying transient protoplast assays and overexpression evaluation in wild-type plants.7-Dehydrocholesterol Technical Information In protoplasts, ARR14 and ARR20 stimulated a luciferase reporter driven by a concatamerized type-B binding web page (TWO Element OUTPUT SENSOR::LUC) within a cytokinin-dependent manner, whereas ARR19 stimulated expression of TWO Component OUTPUT SENSOR::LUC in a cytokininindependent manner, as we saw with ARR18 usingPlant Physiol.PMID:23892407 Vol. 162,Characterization of Type-B ARABIDOPSIS RESPONSE REGULATORSthe ARR6::LUC reporter (M ler and Sheen, 2008; Z cher et al., 2013). In a separate protoplast.