Showing posts with label enhances. Show all posts
Showing posts with label enhances. Show all posts

Monday, 19 August 2013

Geneticists show the COPIA-R7 transposon enhances the immunity of its host against a pathogenic microorganism

Main Category: Genetics
Article Date: 19 Aug 2013 - 1:00 PDT Current ratings for:
Geneticists show the COPIA-R7 transposon enhances the immunity of its host against a pathogenic microorganism
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Transposons are DNA elements that can multiply and change their location within an organism's genome. Discovered in the 1940s, for years they were thought to be unimportant and were called "junk DNA." Also referred to as transposable elements and jumping genes, they are snippets of "selfish DNA" that spread in their host genomes serving no other biological purpose but their own existence.

Now Tokuji Tsuchiya and Thomas Eulgem, geneticists at the University of California, Riverside, challenge that understanding. They report online in the Proceedings of the National Academy of Sciences that they have discovered a transposon that benefits its host organisms.

Working on the model plant Arabidopsis, they found that the COPIA-R7 transposon, which has jumped into the plant disease resistance gene RPP7, enhances the immunity of its host against a pathogenic microorganism that is representative of a large group of fungus-like parasites that cause various detrimental plant diseases.

"We provide a new example for an 'adaptive transposon insertion' event - transposon insertions that can have beneficial effects for their respective host organisms - and uncover the mechanistic basis of its beneficial effects for plants," said Thomas Eulgem, an associate professor of plant cell biology and the senior author of the research paper. "While it has been known for a while that transposon insertions can have positive effects for their respective host organisms and accelerate evolution of their hosts, cases of such adaptive transposon insertions have been rarely documented and are, so far, poorly understood."

The COPIA-R7 transposon affects RPP7 by interfering with the latter's epigenetic code. In contrast to the well known 4-letter genetic DNA code, which provides instructions for the synthesis of proteins, the "epigenetic code" defines the activity states of genes and determines to what extent their genetic information is utilized. Eulgem explained that the transposition of transposons is typically inhibited by epigenetic silencing signals associated with their DNA. Such epigenetic signals are like molecular "flags" or "tags" that are attached to special proteins, around which DNA is wrapped.

A type of molecular flag, referred to as H3K9me2, prohibits transposons from being active and jumping in their host genomes.

"An exciting aspect of our work is that H3K9me2 signals associated with COPIA-R7 have acquired a completely new meaning in RPP7 and promote the activity of this disease-resistance gene," said Eulgem, a member of UC Riverside's Center for Plant Cell Biology. "By modulating levels of this silencing signal in RPP7, plants can adjust the activity of this disease resistance gene.

"Silencing of transposon activity is a complex process that is based on the interplay between different types of epigenetic signals," Eulgem continued. "Typically H3K9me2 is of critical importance for transposon silencing. However, we found H3K9me2 is not important for COPIA-R7 silencing, perhaps because this type of epigenetic signal has acquired a different function within the RPP7 gene. While we found H3K9me2 to promote RPP7 activity, it seems to have lost its function for COPIA-R7 silencing."

Arabidopsis plants use H3K9me2-mediated messenger RNA processing to accurately set RPP7 activity to precisely defined levels. In principle, scientists interested in crop improvement can now use the UCR discovery to design new types of molecular switches based on H3K9me2-mediated messenger RNA processing. Using standard molecular biological methods, transposon sequences that are naturally associated with this epigenetic signal can be inserted into suitable genes and thereby alter the activity levels of these genes.

"Our results are critical for the basic understanding of how transposons can affect the evolution of their hosts - something not well understood at this time," said Tokuji Tsuchiya, the first author of the research paper and an assistant specialist in Eulgem's lab. "Besides this impact on basic research, the epigenetic mechanism we discovered can possibly be utilized for biotechnological crop improvement. In principle, the switch mechanism we discovered can be applied to all crop species that can be genetically modified."

Next, Eulgem plans to expand his lab's research to how plants use the modulation of H3K9me2 levels at COPIA-R7 to dynamically adjust RPP7 activity when they are attacked by a pathogenic microorganism and to explore if this mechanism also applies to additional genes.

"It would make sense to assume that at other transposons, H3K9me2 levels are also modulated during immune responses and that this epigenetic mark affects the activity of other genes that are important for plant immunity," Eulgem said. "If this is true, we have uncovered a completely new genetic - or epigenetic - mechanism that allows plants to sense that they are under pathogen attack and to initiate appropriate immune responses."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our genetics section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

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University of California - Riverside. "Geneticists show the COPIA-R7 transposon enhances the immunity of its host against a pathogenic microorganism." Medical News Today. MediLexicon, Intl., 19 Aug. 2013. Web.
19 Aug. 2013. APA
University of California - Riverside. (2013, August 19). "Geneticists show the COPIA-R7 transposon enhances the immunity of its host against a pathogenic microorganism." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/264954.php.

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'Geneticists show the COPIA-R7 transposon enhances the immunity of its host against a pathogenic microorganism'

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Monday, 5 August 2013

Removing a protein enhances defense against bacteria staphylococcus aureus in CGD mice

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: Immune System / Vaccines;  Blood / Hematology
Article Date: 05 Aug 2013 - 0:00 PDT Current ratings for:
Removing a protein enhances defense against bacteria staphylococcus aureus in CGD mice
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Deletion of a protein in white blood cells improves their ability to fight the bacteria staphylococcus aureus and possibly other infections in mice with chronic granulomatous disease (CGD), according to a National Institutes of Health study. CGD, a genetic disorder also found in people, is marked by recurrent, life-threatening infections. The study's findings appear online in The Journal of Clinical Investigation.

A team of researchers from NIH's National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) compared three groups: CGD-afflicted mice with the protein Olfm4; CGD-afflicted mice in which the protein had been deleted, and healthy mice in which the protein had been deleted. Olfm4, also known as olfactomedin 4, is sometimes helpful in limiting tissue damage but can also hinder white blood cells' ability to kill bacteria.

The researchers found that the white blood cells in mice without the protein could better withstand staphylococcus aureus infection, a major threat to patients with CGD.

"Although treatment for CGD has greatly improved over the past several years, the disease remains challenging," said Dr. Wenli Liu, staff scientist and lead author. "Our research suggests a novel strategy that might pave the way toward developing new treatments to fight against common and often deadly infections."

The results also suggest another potential method to treat methicillin-resistant staphylococcus aureus (MRSA) and other drug-resistant bacteria in patients without CGD, used alongside other therapies. MRSA is a strain of bacteria that has become resistant to antibiotics most often used to treat staph infections. Most commonly contracted in hospitals, MRSA represents a significant public health threat.

"Over the years, MRSA and other bacteria have evolved to be resistant to many antibiotics," said Griffin P. Rodgers, M.D., NIDDK director and study lead. "This study suggests an alternative approach to combat infection by strengthening white blood cell capabilities from within the cells, in addition to resorting to traditional antibiotic treatment."

The research group is now investigating how changing Olfm4 levels in human cells enhances immunity to and from a variety of drug-resistant bacteria. The findings may put researchers closer to developing drug treatment for people, possibly through development of an antibody or small molecule that could inhibit Olfm4 activity.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject.

The study was supported by the Intramural Research Program at NIDDK. Administrative and technical support were provided by the National Heart, Lung, and Blood Institute and the National Institute of Allergy and Infectious Diseases, both part of NIH.

NIH/National Institute of Diabetes and Digestive and Kidney Diseases

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

NIH/National Institute of Diabetes and Digestive a. "Removing a protein enhances defense against bacteria staphylococcus aureus in CGD mice." Medical News Today. MediLexicon, Intl., 5 Aug. 2013. Web.
5 Aug. 2013. APA

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'Removing a protein enhances defense against bacteria staphylococcus aureus in CGD mice'

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All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

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Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.



View the original article here