CAMBIA Reveals Open Source Plant Biotech For All • Japanese

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Research Findings
Australia
CAMBIA Reveals
Open Source Plant Biotech For All
S
cientists have found a fresh method of transferring genes into agricultural
crops without patent laws preventing this discovery from being shared
with the rest of the world. A paper recently published in the journal Nature
reported that three bacteria are just as good at delivering DNA as the traditional
carrier.
The authors from the Center for the Application of Molecular Biology to
International Agriculture (CAMBIA), a non-profit, Australian-based organization
that licenses a variety of technologies under an open source principle, say this
technology can be shared.
Author and molecular geneticist Dr. Richard Jefferson, CAMBIA’s founder
and chief executive officer, described the paper as the world’s first “explicit open
source” biotechnology toolkit. He sees it as an alternative approach to plant
biotechnology — a technology that is not being applied as widely as it could
due to restriction by an abundance of patent laws.
Plant biotechnology can involve transferring new or modified genes into
plants to make them immune to certain pests or diseases. For instance, Jefferson
said it may be possible, in the long term, to introduce genes that turn an ear of
corn bright red as an indication to farmers of the apt time to water or fertilize
them. The genes are introduced via bacteria, which infect the plant and, like a
Trojan horse, deliver DNA into its cells.
Up till now, the most common method of doing this has been to use
Agrobacterium tumefaciens, a pathogen that causes tumors to grow on plants.
However, the use of Agrobacterium is limited by patent laws. Jefferson said this
makes the technology expensive and inaccessible to those who could most
benefit from it, such as public research bodies, rural communities and Third
World countries.
The researchers showed that gene transfer works using strains of Rhizobium,
Sinorhizobium, and Mesorhizobium. Unlike Agrobacterium, these bacteria are
not pathogens, which means that they may be more easily accepted by plants.
Neither are they bound by commercial patent laws.
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Research Findings
The licenses to the new method of DNA transfer, dubbed TransBacter
technology, are being administered by CAMBIA. Jefferson said the Center would
allow the technology to be shared with anyone provided that all improvements
and biosafety information are shared, preventing it from being “hijacked” by
large biotechnology companies.
CAMBIA also announced the launch of BioForge, an online research site
based on the principle of open source technology.
About CAMBIA
CAMBIA is financed by philanthropic organizations, national and international
research funding bodies, royalties derived from licensing its own technologies,
and limited commercial R&D partnerships. CAMBIA conducts research in areas of
strategic importance for sustainable agriculture. In general, CAMBIA is developing
tools capable of enabling more innovation in agricultural production through the
use of molecular biology. There are two main research programs in CAMBIA,
Molecular Technologies and Functional Genomics.
Contact Details:
CAMBIA
Address: Clunies Ross Street at Dickson Road, Black
Mountain, GPO Box 3200, Canberra ACT
2601, Australia
Tel:
+61 2 6246 4500
Fax:
+61 2 6246 4501
Email: [email protected]
URL:
www.cambia.org
Rhizobium is a type of bacterium that lives in the soil and around and inside of the roots of certain
plants (legumes). This is Rhizobium in its free-living state in soil, surrounded by a halo of protective
covering called a capsule. The slimy capsule, made of exopolysaccharide, protects the rhizobium
from drying out. It also helps the bacterium stick to root hairs during other stages of its life cycle,
when rhizobium forms a symbiotic partnership with plants like clover.
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Research Findings
Japan
Japanese Researchers Find
Susceptibility Gene for
Arthritis
A
susceptibility gene to osteoarthritis, a painful degenerative joint disease,
has been identified by RIKEN researchers in the Laboratory for Bone
and Joint Diseases, Tokyo. Led by Shiro Ikegawa, they identified an
asporin gene (ASPN) as one of the causative genes. Further, the group has found
that the risk of osteoarthritis can be doubled when an ASPN allele provides
a polymorphism, namely 14 aspartic acid repeats. The latest discovery may
contribute to the development of new treatments and drugs for osteoarthritis.
The team found a polymorphism (D14) in the asporin gene (ASPN) that
occurs more commonly in patients with osteoarthritis. Asporin suppresses TGF-β
expression in chondrogenesis (cartilage generative and regenerative processes) in
vitro, which is necessary to maintain healthy cartilage in joints. The D14 allele
presents the strongest inhibitory effect among all alleles of asporin, preventing
or impairing chondrogenesis.
Asporin, a member of the SLRP (small leucine rich protein) protein family,
contributes to ECM formation as a negative regulator of chondrocyte differentiation
and binds to TGF-β , a growth factor for cartilage. Therefore, the researchers
suspected that naturally occurring variations in APSN might affect predispose
individual susceptibility to osteoarthritis.
The next step would be to delineate the functional relationships of asporin
and the effects of the various D-repeats on those relationships. Understanding how
asporin contributes to osteoarthritis requires first understanding how the protein
interacts with other extracellular matrix proteins and TGF-β activity, which in
turn could lead to novel therapeutic treatments.
About osteoarthritis
Over 5% of the global population, including more than 7 million people in Japan,
are diagnosed with osteoarthritis, which is characterized as the gradual decline of
cartilage until bone grates against bone. Osteoarthritis (OA) is the most common
form of bone and joint diseases. When the cartilage cushioning the bones breaks
down, the pain can often lead to immobility, restricting activity and impacting
an individual’s the quality of life. The etiology is unclear but it is considered a
polygenetic disease, where a combination of genetic and environmental factors
contributes to its onset and progression. Osteoarthritis still lacks reliable treatments
that alleviate symptoms or halt progression.
Articular cartilage is a slick layer of proteins that lubricate and cushion
the bone against abrasion in the joint. This viscoelasticity is maintained by
the extracellular matrix (ECM) that builds and rebuilds the articular cartilage.
Degeneration of the cartilage may result from impairment in this matrix, processes
involved, or in gene transcription.
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Research Findings
About RIKEN
The Riken Institute was first founded in 1917 (Taisho 6) as a private research
foundation known as “RIKEN”. In 2003, it was reorganized as an Independent
Administrative Institution under the Ministry of Education, Culture, Sports, Science
and Technology, since when it has engaged in wide-ranging research activities
that span basic to applied science.
The objectives of RIKEN are to conduct comprehensive research in science
and technology (excluding only humanities and social sciences) under the “RIKEN
Law”, and to disseminate the results of its scientific research and technological
developments. RIKEN carries out high level experimental and research work in a
wide range of fields, including physics, chemistry, medical science, biology, and
engineering extending from basic research to practical application.
Contact Details:
RIKEN
Address: 2-1 Hirosawa, Wako, Saitama 351-0198 Japan
Tel:
+81 48 462 1111
Fax:
+81 48 462 1554
URL:
www.riken.jp/engn/index.html
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Kizawa et al., An aspartic acid repeat polymorphism in asporin inhibits chondrogenesis and
increases susceptibility to osteoarthritis, Nature Gen 37:138–144, 2005.
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Research Findings
Korea
World’s First
Stroke Medicine
K
orean researchers have developed a new stroke drug, called Neu 2000,
that promises a higher chance of recovery for a stroke victim. Currently,
there is no medicine approved officially for use worldwide in the
treatment of stroke.
A stroke occurs when a part of the brain is deprived of blood supply due to a
blood clot or bursting of a blood vessel. Researchers say Neu 2000 works in two
ways: first by protecting cerebral cells from reperfusion damage as it neutralizes
toxins generated by oxidation or decomposition during a stroke, and second
as an anticoagulant to prevent blood clots. The drug lasts up to 36 hours while
current drugs only last for three hours. Hence, Neu 2000 buys crucial time for
stroke patients to reach a hospital.
The research team from Ajou University's School of Medicine, led by Dr.
Gwag Byoung-joo, announced on 24 January 2005 that they had completed animal
testing and tests have been successful. “After 10 years of domestic research and
experiments, we are able to start clinical experiments in the US in September,” said
Dr. Gwag. The clinical trials will be conducted by Quintiles Transnational under
the direction of Chung Y. Hsu, Dean of the Medical College of Taipei University.
The experiments will be funded by Amkor, an American funding company and
the technology will be transferred to Merck, A US Pharmaceutical firm in 2007
after finishing clinical trials. Merck will develop Neu 2000 and plans are to start
selling the world's first stroke medicine around 2010–2012.
At the moment, there is only one drug for treating stroke. Called Edarabone,
it was developed by a Japanese pharmaceutical company and is approved for use
in Japan only, but has shown lethal side-effects, including liver failure. Developers
of the new drug say so far experiments with Neu 2000 have not shown serious
side-effects. “Neu 2000 has already got patents in the US And Europe, and it
is 1000 times more efficient in preventing the action of oxygen free radicals,”
Dr. Gwag said. With the sales of Edarabone in Japan reaching 300 billion won
(US$300 million) each year alone, global sales are expected to be 3 trillion
won (US$3 billion) for the new drug as there are an estimated 40 million stroke
patients worldwide.
Contact Details:
Kwag Byoung-Joo
Email: [email protected]
URL: wwwold.ajou.ac.kr/~bdrc/peo/Byoung-Joo.htm
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