The ACAULIS5 (ACL5) gene encodes a polyamine synthase producing an isomer of spermine named thermospermine. The acl5 loss-of-function mutant, also known as thickvein, is dwarf and characterized by the formation of an increased number of veins and vascular elements in leaves and stems (Hanzawa et al., 1997, 2000; Clay et al., 2005). It has been proposed that ACL5 controls xylem specification by preventing premature cell death of tracheary elements (Knott et al., 2007; Muniz et al., 2008). Here we show that higher levels of ACL5, likely resulting in increased thermospermine concentration, significantly delay or completely inhibit the differentiation of procambial cells into tracheary elements in leaf as well as in primary and secondary vasculature of stem and hypocotyl. We also show that ACL5 is directly regulated in a positive manner by the HD-ZIPIII transcription factor ATHB8, whose expression marks preprocambial cell state and accurately predicts sites of leaf vein formation (Donner et al., 2009). On the other hand, ATHB8 gene expression is upregulated in acl5, suggesting that the vascular defects observed in this mutant may in part depend on enhanced HD-ZIPIII activity (Baima et al, 2001; Imai et al. 2006; Kakhei et al., 2008). A careful genetic analysis of acl5 in combination with athb8 and other hd-zipiii mutants indicated that some of the developmental defects caused by the lack of ACL5 activity are indeed abolished by the loss of the HD-ZIPIII transcription factors. Taken together our data indicate that the HD-ZIPIII and ACL5 genes are required to sustain a negative feedback loop involved in the regulation of vascular development.
A negative feedback regulatory loo controlling vascular development
Ida Ruberti;
2012
Abstract
The ACAULIS5 (ACL5) gene encodes a polyamine synthase producing an isomer of spermine named thermospermine. The acl5 loss-of-function mutant, also known as thickvein, is dwarf and characterized by the formation of an increased number of veins and vascular elements in leaves and stems (Hanzawa et al., 1997, 2000; Clay et al., 2005). It has been proposed that ACL5 controls xylem specification by preventing premature cell death of tracheary elements (Knott et al., 2007; Muniz et al., 2008). Here we show that higher levels of ACL5, likely resulting in increased thermospermine concentration, significantly delay or completely inhibit the differentiation of procambial cells into tracheary elements in leaf as well as in primary and secondary vasculature of stem and hypocotyl. We also show that ACL5 is directly regulated in a positive manner by the HD-ZIPIII transcription factor ATHB8, whose expression marks preprocambial cell state and accurately predicts sites of leaf vein formation (Donner et al., 2009). On the other hand, ATHB8 gene expression is upregulated in acl5, suggesting that the vascular defects observed in this mutant may in part depend on enhanced HD-ZIPIII activity (Baima et al, 2001; Imai et al. 2006; Kakhei et al., 2008). A careful genetic analysis of acl5 in combination with athb8 and other hd-zipiii mutants indicated that some of the developmental defects caused by the lack of ACL5 activity are indeed abolished by the loss of the HD-ZIPIII transcription factors. Taken together our data indicate that the HD-ZIPIII and ACL5 genes are required to sustain a negative feedback loop involved in the regulation of vascular development.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
