This is an odd item but it shows us how well we are along in
mastering natural wood growth and yes it would be nice to enhance
woods viability as a source of fiber and also as a chemical feedstock
and even biofuel.
It is tricks like this that give hope that those objectives are
possible.
Wood science itself is settling into a completely new paradigm in
which rapid tropical growth is selected to provide ample commercial
fiber. In the long term scant use will be made of the old wild wood
and most of that will at least be groomed. Thus we have witnessed a
general recovery taking place most everywhere.
Research on Wood
Formation Sheds Light on Plant Biology
Released: 8/23/2012
1:30 PM EDT
Newswise —
Scientists at North Carolina State University have discovered a
phenomenon never seen before in plants while studying molecular
changes inside tree cells as wood is formed.
In research published
online in Proceedings of the National Academy of Sciences the
week of Aug. 20, the team found that one member of a family of
proteins called transcription factors took control of a cascade of
genes involved in forming wood, which includes a substance called
lignin that binds fibers together and gives wood its strength.
The controller
protein regulated gene expression on multiple levels, preventing
abnormal or stunted plant growth. And it did so in a novel way.
The controller, a
spliced variant of the SND1 family, was found in the cytoplasm
outside the cell nucleus. This is abnormal, because transcription
factor proteins are always in the nucleus. But when one of the
four other proteins in its family group was present, the spliced
variant was carried into the nucleus, where it bound to the family
member, creating a new type of molecule that suppressed the
expression of a cascade of genes.
“This is nothing
that’s been observed before in plants,” says Dr. Vincent Chiang,
co-director of NC State’s Forest Biotechnology Group with Dr. Ron
Sederoff. Chiang’s research team was the first to produce a
transgenic tree with reduced lignin. High lignin levels are desirable
for lumber, but lignin is removed during the process of making paper
or manufacturing biofuels.
Chiang, a professor in
the College of Natural Resources, described the team’s finding as
the long-sought path to understanding the hierarchy of gene
regulation for wood formation.
Lead authors are Dr.
Quanzi Li, senior research associate, who discovered the controller
protein, and doctoral student Ying-Chung Lin, who carried out
extensive experimental work, demonstrating with Li that the
controller protein was carried into the nucleus.
The research was
funded with a grant from the U.S. Department of Energy's Office of
Biological and Environmental Research.
Note to editors: An
abstract of the paper follows.
“Splice Variant of the SND1 Transcription Factor Is a Dominant Negative of SND1 Members and Their Regulation in Populus trichocarpa”
Published: Online the
week of Aug. 20 in Proceedings of the National Academy of Sciences
Authors: Quanzi Li,
Ying-Chung Lin, Ying-Hsuan Sun, Jian Song, Hao Chen, Xing-Hai Zhang,
Ronald R. Sederoff, and Vincent L. Chiang. All are members of the
Forest Biotechnology Group in the Department of Forestry and
Environmental Resources at North Carolina State University, except
for Xing-Hai Zhang, who is with the Department of Biological Sciences
at Florida Atlantic University.
Abstract: Secondary
Wall-Associated NAC Domain 1s (SND1s) are transcription factors (TFs)
known to activate a cascade of TF and pathway genes affecting
secondary cell wall biosynthesis (xylogenesis) in Arabidopsis and
poplars. Elevated SND1 transcriptional activation leads to ectopic
xylogenesis and stunted growth. Nothing is known about the upstream
regulators of SND1. Here we report the discovery of a
stem-differentiating xylem (SDX)-specific alternative SND1 splice
variant, PtrSND1-A2IR, that acts as a dominant negative of SND1
transcriptional network genes in Populus trichocarpa. PtrSND1-A2IR
derives from PtrSND1-A2, one of the four fully spliced PtrSND1 gene
family members (PtrSND1-A1, -A2, -B1, and -B2). Each full-size
PtrSND1 activates its own gene, and all four full-size members
activate a common MYB gene (PtrMYB021). PtrSND1-A2IR represses the
expression of its PtrSND1 member genes and PtrMYB021. Repression of
the autoregulation of a TF family member by its only splice variant
has not previously been reported in plants. PtrSND1-A2IR lacks DNA
binding and transactivation abilities but retains dimerization
capability. PtrSND1-A2IR is localized exclusively in cytoplasmic
foci. In the presence of any full-size PtrSND1 member, PtrSND1-A2IR
is translocated into the nucleus exclusively as a heterodimeric
partner with full-size PtrSND1s. Our findings are consistent with a
model in which the translocated PtrSND1-A2IR lacking DNA-binding and
transactivating abilities can disrupt the function of full-size
PtrSND1s, making them nonproductive through heterodimerization, and
thereby modulating the SND1 transcriptional network. PtrSND1-A2IR may
contribute to transcriptional homeostasis to avoid deleterious
effects on xylogenesis and plant growth.
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