Biology Reference
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and secondary xylem of hypocotyls in Arabidopsis. Dominant repression
of NST1 and NST3/SND1 or the double knockout of nst1 and nst3/snd1
suppress the formation of SW specifically in interfascicular and vascular
fibres but not in xylem vessels (
Mitsuda and Ohme-Takagi, 2008; Mitsuda
et al., 2007; Yamaguchi, 2010
). However, SND1 loss-of-function mutants
have no clear secondary wall phenotype and overexpressors lead to massive
ectopic deposition of lignified SW in leaves but also to a drastic inhibition of
secondary cell thickening of fibres (
Zhong et al., 2006
). This later phenotype
was also observed by
Ko et al. (2007)
. In their case, overexpression of SND1
(called ANAC012) led to a reduction of secondary cell-wall deposition in
xylary fibres and to a slight increase in xylem vessel cells in Arabidopsis.
Intriguingly, the two groups came up with opposite interpretations.
Zhong
et al. (2006)
considered that SND1 is a key transcriptional activator of
secondary wall biosynthesis in fibres whereas
Ko et al. (2007)
concluded
that ANAC012 (SND1) acts as a negative regulator of secondary wall
thickening in xylary fibre. The overexpression phenotype in fibres is indeed
odd and may indicate that a defined level of SND1 is critical for the normal
deposition of SW in fibres. The importance of expression thresholds in TF
studies has also been pointed out in other studies including those on another
NAC factor, SND2 (
Hussey et al., 2011
).
In contrast to Arabidopsis which harbours 3 NST genes, there is only a
single fibre-specific SWN TF, MtNST1, in the model legume Medicago
truncatula, which orchestrates multiple features of cell wall development in
different tissues (
Zhao et al., 2010a
). Loss of MtNST1 function resulted in
reduced lignin content, associated with reduced expression of most lignin
biosynthetic genes, and a smaller reduction in cell wall polysaccharide con-
tent, associated with reduced expression of putative cellulose and hemicellu-
lose biosynthetic genes. Similarly, a loss-of-function point mutation in the
MtNST1 gene, leads to an absence of lignification in interfascicular fibres
(
Wang et al., 2011
).
B. NAC
S
REGULATING SWS IN XYLEM VESSELS
In xylem vessels, the NAC domain TFs VND6 and VND7 control both
secondary wall development and programmed cell death (PCD) of the vessels
in both root and shoot tissues (
Kubo et al., 2005; Yamaguchi et al., 2008
).
Although loss of function of each VND does not lead to any phenotype,
VND6 and VND7 can independently complement the nst1x snd1 double
mutant phenotype in Arabidopsis (
Zhong et al., 2010b, 2010c
). VND6 and
VND7 can act as key regulators of the differentiation of two different types
of xylem vessels (metaxylem and protoxylem) both in Arabidopsis and in
