R
Robert Karl Sto
Guest
Same Tools, Different Boxes Convergent evolution plays out in plant and animal innate immunity By
Philip Hunter
As life's diversity demonstrates, nature has a pretty large toolbox for designing adaptations. While
in many ways an efficient builder, it often reuses blueprints, even if not starting with the same
tools. Analogous wing structures in bird and bat suggest a why-mess-with-success ethos. New World
cacti and desert-dwelling Euphorbiaceae in the Old World share protective spines and
photosynthesizing stems even though the last common ancestor predates such modifications.
Beyond structural adaptations, researchers are investigating convergent evolution at the molecular
level, and this may allow for broader comparisons even between plants and animals. Both, of course,
share the building blocks and fundamental biochemistry that evolved before the two kingdoms
presumably diverged from common single-celled ancestors. But with their radically different cell
structures, plants and animals were thought to have pursued largely independent evolutionary routes.
Such disparity was reflected in the lack of interaction between the respective research communities.
But much is changing, especially with respect to the study of innate immunity, which turns out to
involve strikingly similar mechanisms in both plants and animals. One can find resemblances in the
receptors that recognize pathogenic components such as lipopolysaccharide; in the signaling systems
that initiate responses through kinase cascades; and in the defense mechanisms, including reactive
molecules such as nitric oxide, says Jonathan Jones, senior scientist at the Sainsbury Laboratory of
the John Innes Centre in Norwich, UK.
Moreover, says Jones, autoimmune disorders can develop in plants as well as animals. In many cases,
researchers consider plant and animal innate-immunity analogs to have evolved independently,
because the underlying genes involved are radically different. Here, convergence is occurring
purely at the functional level, according to Daniel Klessig, president and CEO of Boyce Thompson
Institute (BTI) for Plant Research in Ithaca, NY. But now, say some, both functional and genetic
similarities between plant and animal immunity are leading to cross-pollination between the
respective research fields.
Read the rest at TheScientist.com http://www.the-scientist.com/yr2004/feb/research4_040216.html
Comment: Could viral vectors be suspected here?
When the Lights Went On for COP9 A protein's role in ubiquitin-mediated proteasomal degradation
plants the seed for big ideas By Eugene Russo
It doesn't take a green thumb to predict what happens to plants left in the dark: They wither. But
in the late 1980s and early 1990s, researchers, including people in Xing-**** Deng's Yale
University lab, stumbled upon a group of intriguing Arabidopsis mutants that seemed to defy
intuition. If provided the right nutrition, these plants could retain a shape, form, and cellular
state similar to those grown in ample light for weeks, and even months, of sustained darkness. Some
could even flower.
In 1994, Deng's group identified COP9, one of the genes responsible for this impressive feat.1 After
doing some bioinformatics digging and biochemistry work, they found that the COP9 gene encoded a
novel protein that was part of a larger protein complex later called the COP9 signalosome (CSN).
As it turns out, the CSN does more than regulate plant responses to light; Deng's lab and others
subsequently found signalosome homologs in mammals and other species. "There were a variety of
different facts floating around and a lot of speculation," says Svetlana Lyapina, a Hot Paper first
author and now a manager of strategy and corporate development at Amgen, Thousand Oaks, Calif. "But
there was no sort of unified theory of what signalosome does and how it does it."
This issue's Hot Papers2,3 link CSN function to ubiquitin ligases, a family that includes hundreds
of known key regulators of inflammation and the cell cycle. Approaching signalosome function from
different fields (biochemistry and plant genetics) and with different agendas, the two groups found
that in plants,2 yeast, and mammalian cells,3 the CSN directly interacts with an ubiquitin ligase
complex that mediates proteasomal degradation of proteins involved in cell cycle and development.
"Basically, this provided a biochemical mechanism, a biochemical connection for how COP9 signalosome
is involved in protein degradation mediated by the proteasome," says Deng. The complexes are now
known to be major signaling processors in the cell, and they may be relevant in treating diseases
such as cancer. Thus, with the shade drawn, a new research window had burst open.
http://www.the-scientist.com/yr2004/feb/hot_040216.html
Posted by Robert Karl Stonjek.
Philip Hunter
As life's diversity demonstrates, nature has a pretty large toolbox for designing adaptations. While
in many ways an efficient builder, it often reuses blueprints, even if not starting with the same
tools. Analogous wing structures in bird and bat suggest a why-mess-with-success ethos. New World
cacti and desert-dwelling Euphorbiaceae in the Old World share protective spines and
photosynthesizing stems even though the last common ancestor predates such modifications.
Beyond structural adaptations, researchers are investigating convergent evolution at the molecular
level, and this may allow for broader comparisons even between plants and animals. Both, of course,
share the building blocks and fundamental biochemistry that evolved before the two kingdoms
presumably diverged from common single-celled ancestors. But with their radically different cell
structures, plants and animals were thought to have pursued largely independent evolutionary routes.
Such disparity was reflected in the lack of interaction between the respective research communities.
But much is changing, especially with respect to the study of innate immunity, which turns out to
involve strikingly similar mechanisms in both plants and animals. One can find resemblances in the
receptors that recognize pathogenic components such as lipopolysaccharide; in the signaling systems
that initiate responses through kinase cascades; and in the defense mechanisms, including reactive
molecules such as nitric oxide, says Jonathan Jones, senior scientist at the Sainsbury Laboratory of
the John Innes Centre in Norwich, UK.
Moreover, says Jones, autoimmune disorders can develop in plants as well as animals. In many cases,
researchers consider plant and animal innate-immunity analogs to have evolved independently,
because the underlying genes involved are radically different. Here, convergence is occurring
purely at the functional level, according to Daniel Klessig, president and CEO of Boyce Thompson
Institute (BTI) for Plant Research in Ithaca, NY. But now, say some, both functional and genetic
similarities between plant and animal immunity are leading to cross-pollination between the
respective research fields.
Read the rest at TheScientist.com http://www.the-scientist.com/yr2004/feb/research4_040216.html
Comment: Could viral vectors be suspected here?
When the Lights Went On for COP9 A protein's role in ubiquitin-mediated proteasomal degradation
plants the seed for big ideas By Eugene Russo
It doesn't take a green thumb to predict what happens to plants left in the dark: They wither. But
in the late 1980s and early 1990s, researchers, including people in Xing-**** Deng's Yale
University lab, stumbled upon a group of intriguing Arabidopsis mutants that seemed to defy
intuition. If provided the right nutrition, these plants could retain a shape, form, and cellular
state similar to those grown in ample light for weeks, and even months, of sustained darkness. Some
could even flower.
In 1994, Deng's group identified COP9, one of the genes responsible for this impressive feat.1 After
doing some bioinformatics digging and biochemistry work, they found that the COP9 gene encoded a
novel protein that was part of a larger protein complex later called the COP9 signalosome (CSN).
As it turns out, the CSN does more than regulate plant responses to light; Deng's lab and others
subsequently found signalosome homologs in mammals and other species. "There were a variety of
different facts floating around and a lot of speculation," says Svetlana Lyapina, a Hot Paper first
author and now a manager of strategy and corporate development at Amgen, Thousand Oaks, Calif. "But
there was no sort of unified theory of what signalosome does and how it does it."
This issue's Hot Papers2,3 link CSN function to ubiquitin ligases, a family that includes hundreds
of known key regulators of inflammation and the cell cycle. Approaching signalosome function from
different fields (biochemistry and plant genetics) and with different agendas, the two groups found
that in plants,2 yeast, and mammalian cells,3 the CSN directly interacts with an ubiquitin ligase
complex that mediates proteasomal degradation of proteins involved in cell cycle and development.
"Basically, this provided a biochemical mechanism, a biochemical connection for how COP9 signalosome
is involved in protein degradation mediated by the proteasome," says Deng. The complexes are now
known to be major signaling processors in the cell, and they may be relevant in treating diseases
such as cancer. Thus, with the shade drawn, a new research window had burst open.
http://www.the-scientist.com/yr2004/feb/hot_040216.html
Posted by Robert Karl Stonjek.