A role for BELLRINGER in cell wall development is supported by loss-of-function phenotypes

Plants over-expressing BLR exhibited a wide range of phenotypes. Some were defective in cell size and demonstrated misregulation of genes predominantly affecting cell wall development. Other lines with more extreme phenotypes failed to generate lateral organs, consistent with BLR repressing transcription in the shoot apex. Cell wall dynamics are also affected in blr mutant plants, and BLR has previously been shown to regulate vascular development in conjunction with BP. We found that when bp and blr were combined with rev, a set of defects was observed that were distinct from those of bp blr lines. In these triple mutants xylem development was most strikingly affected, resulting in an almost complete lack of vessels and xylem parenchyma with secondary thickening.Our data support a role for BLR in ordering the shoot apex and, in conjunction with BP and REV, playing a part in determining the composition and organisation of the vascular system. Microarray analysis strongly indicates that the striking vascular phenotypes of blr bp rev triple mutants and plants over-expressing BLR result from the misregulation of a suite of genes, targets of BLR in wild type plants, that determine cell size and structure in the developing vasculature.BELLRINGER (BLR), also known as VAAMANA, PENNYWISE, LARSON and REPLUMLESS, is a member of the BELL family of homeodomain transcription factors and functions in diverse processes in the development of Arabidopsis[1-5]. BLR was identified independently as a suppresser of the floral homeotic gene AGAMOUS (AG) [5], as a factor required in fruit development for specification of the replum [1] and as a gene necessary for normal phyllotactic patterning [2,4]. BELL transcription factors were shown to enhance DNA binding of maize KNOTTED1 [6], the founding member of the KNOX1 gene family [7], and BLR was subsequently shown to act synergistically with the KNOX1 homeodomain transcription factor BREVIPEDICELLUS (BP) [3]. BLR and KNOX1 proteins heterodim