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High doses of vitamin D rapidly reduce arterial stiffness in overweight/obese, vitamin-deficient African-Americans
Date: January 2, 2018 Source: Medical College of Georgia at Augusta University Summary: In just four months, high-doses of vitamin D reduce arterial stiffness in young, overweight/obese, vitamin-deficient, but otherwise still healthy African-Americans, researchers say.
In just four months, high-doses of vitamin D reduce arterial stiffness in young, overweight/obese, vitamin-deficient, but otherwise still healthy African-Americans, researchers say.
Rigid artery walls are an independent predictor of cardiovascular- related disease and death and vitamin D deficiency appears to be a contributor, says Dr. Yanbin Dong, geneticist and cardiologist at the Georgia Prevention Institute at the Medical College of Georgia at Augusta University.
So researchers looked at baseline and again 16 weeks later in 70 African-Americans ages 13-45 -- all of whom had some degree of arterial stiffness -- taking varying doses of the vitamin best known for its role in bone health.
In what appears to be the first randomized trial of its kind, they found that arterial stiffness was improved by vitamin D supplementation in a dose-response manner in this population, they write in the journal PLOS ONE.
Overweight/obese blacks are at increased risk for vitamin D deficiency because darker skin absorbs less sunlight -- the skin makes vitamin D in response to sun exposure -- and fat tends to sequester vitamin D for no apparent purpose, says Dong, the study's corresponding author.
Participants taking 4,000 international units -- more than six times the daily 600 IUs the Institute of Medicine currently recommends for most adults and children -- received the most benefit, says Dr. Anas Raed, research resident in the MCG Department of Medicine and the study's first author.
The dose, now considered the highest, safe upper dose of the vitamin by the Institute of Medicine, reduced arterial stiffness the most and the fastest: 10.4 percent in four months. "It significantly and rapidly reduced stiffness," Raed says.
Two thousand IUs decreased stiffness by 2 percent in that timeframe. At 600 IUs, arterial stiffness actually increased slightly -- .1 percent -- and the placebo group experienced a 2.3 percent increase in arterial stiffness over the timeframe.
They used the non-invasive, gold standard pulse wave velocity to assess arterial stiffness. Reported measures were from the carotid artery in the neck to the femoral artery, a major blood vessel, which supplies the lower body with blood. The American Heart Association considers this the primary outcome measurement of arterial stiffness.
When the heart beats, it generates a waveform, and with a healthy heart and vasculature there are fewer and smaller waves. The test essentially measures the speed at which the blood is moving, and in this case, fast is not good, Raed says.
"When your arteries are more stiff, you have higher pulse wave velocity, which increases your risk of cardiometabolic disease in the future," says Raed.
The varying doses, as well as the placebo participants took, were all packaged the same so neither they or the investigators knew which dose, if any, they were getting until the study was complete. Both placebo and supplements were given once monthly -- rather than daily at home -- at the GPI to ensure consistent compliance.
Dong was also corresponding author on a study published in 2015 in the journal BioMed Central Obesity that showed, in this same group of individuals, both 2,000 and 4,000 IUs restored more desirable vitamin D blood levels of 30 nanograms per milliliter.
The 4,000 upper-limit dose restored healthy blood level quicker -- by eight weeks -- and was also better at suppressing parathyroid hormone, which works against vitamin D's efforts to improve bone health by absorbing calcium, they reported.
While heart disease is the leading cause of death in the United States, according to the Centers for Disease Control and Prevention, blacks have higher rates of cardiovascular disease and death than whites and the disease tends to occur earlier in life. The authors write that arterial stiffness and vitamin D deficiency might be potential contributors.
While just how vitamin D is good for our arteries isn't completely understood, it appears to impact blood vessel health in many ways. Laboratory studies have shown that mice missing a vitamin D receptor have higher activation of the renin-angiotensin-aldosterone system, says Raed. Activation of this system increases blood vessel constriction, which can contribute to arterial stiffness. Vitamin D also can suppress vascular smooth muscle cell proliferation, activation of garbage-eating macrophages and calcification formation, all of which can thicken blood vessel walls and hinder flexibility. Vitamin D also reduces inflammation, an underlying mechanism for obesity related development of coronary artery disease, says Raed.
Now it's time to do a larger-scale study, particularly in high-risk populations, and follow participants' progress for longer periods, Dong and Raed say. "A year would give us even more data and ideas," Raed adds.
Dong notes that pulse wave velocity and blood pressure measures are complementary but not interchangeable. "We think maybe in the future, when you go to your physician, he or she might check your arterial stiffness as another indicator of how healthy you are," Raed says.
There were no measurable differences in weight or blood pressure measurements over the 16-week study period.
The Institute of Medicine currently recommends a daily intake of 800 IUs of vitamin D for those age 70 and older. For adolescents and adults, they recommend 4,000 IUs as the upper daily limit; 2,000 was a previous upper limit.
More than 80 percent of Americans, the majority of whom spend their days indoors, have vitamin D insufficiency or deficiency. Dong, an expert in vitamin D and a professor in the MCG Department of Population Health Sciences, says about 15 minutes daily in the "young" sun -- between 10 a.m. and 2 p.m. -- but before your skin starts to get pink, is the best source of vitamin D.
Foods like milk, milk products like cheese and yogurt, fatty fish like mackerel and sardines, some greens like kale and collards and fortified cereals also are good sources. The researchers say a vitamin D supplement is an inexpensive and safe option for most of us.
Story Source:
Materials provided by Medical College of Georgia at Augusta University. Original written by Toni Baker. Note: Content may be edited for style and length.
Journal Reference:
Anas Raed, Jigar Bhagatwala, Haidong Zhu, Norman K. Pollock, Samip J. Parikh, Ying Huang, Robyn Havens, Ishita Kotak, De-Huang Guo, Yanbin Dong. Dose responses of vitamin D3 supplementation on arterial stiffness in overweight African Americans with vitamin D deficiency: A placebo controlled randomized trial. PLOS ONE, 2017; 12 (12): e0188424 DOI: 10.1371/journal.pone.0188424
Cite This Page:
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Medical College of Georgia at Augusta University. "High doses of vitamin D rapidly reduce arterial stiffness in overweight/obese, vitamin-deficient African-Americans." ScienceDaily. ScienceDaily, 2 January 2018. <www.sciencedaily.com/releases/2018/01/180102114147.htm>.
In just four months, high-doses of vitamin D reduce arterial stiffness in young, overweight/obese, vitamin-deficient, but otherwise still healthy African-Americans, researchers say.
Rigid artery walls are an independent predictor of cardiovascular- related disease and death and vitamin D deficiency appears to be a contributor, says Dr. Yanbin Dong, geneticist and cardiologist at the Georgia Prevention Institute at the Medical College of Georgia at Augusta University.
So researchers looked at baseline and again 16 weeks later in 70 African-Americans ages 13-45 -- all of whom had some degree of arterial stiffness -- taking varying doses of the vitamin best known for its role in bone health.
In what appears to be the first randomized trial of its kind, they found that arterial stiffness was improved by vitamin D supplementation in a dose-response manner in this population, they write in the journal PLOS ONE.
Overweight/obese blacks are at increased risk for vitamin D deficiency because darker skin absorbs less sunlight -- the skin makes vitamin D in response to sun exposure -- and fat tends to sequester vitamin D for no apparent purpose, says Dong, the study's corresponding author.
Participants taking 4,000 international units -- more than six times the daily 600 IUs the Institute of Medicine currently recommends for most adults and children -- received the most benefit, says Dr. Anas Raed, research resident in the MCG Department of Medicine and the study's first author.
The dose, now considered the highest, safe upper dose of the vitamin by the Institute of Medicine, reduced arterial stiffness the most and the fastest: 10.4 percent in four months. "It significantly and rapidly reduced stiffness," Raed says.
Two thousand IUs decreased stiffness by 2 percent in that timeframe. At 600 IUs, arterial stiffness actually increased slightly -- .1 percent -- and the placebo group experienced a 2.3 percent increase in arterial stiffness over the timeframe.
They used the non-invasive, gold standard pulse wave velocity to assess arterial stiffness. Reported measures were from the carotid artery in the neck to the femoral artery, a major blood vessel, which supplies the lower body with blood. The American Heart Association considers this the primary outcome measurement of arterial stiffness.
When the heart beats, it generates a waveform, and with a healthy heart and vasculature there are fewer and smaller waves. The test essentially measures the speed at which the blood is moving, and in this case, fast is not good, Raed says.
"When your arteries are more stiff, you have higher pulse wave velocity, which increases your risk of cardiometabolic disease in the future," says Raed.
The varying doses, as well as the placebo participants took, were all packaged the same so neither they or the investigators knew which dose, if any, they were getting until the study was complete. Both placebo and supplements were given once monthly -- rather than daily at home -- at the GPI to ensure consistent compliance.
Dong was also corresponding author on a study published in 2015 in the journal BioMed Central Obesity that showed, in this same group of individuals, both 2,000 and 4,000 IUs restored more desirable vitamin D blood levels of 30 nanograms per milliliter.
The 4,000 upper-limit dose restored healthy blood level quicker -- by eight weeks -- and was also better at suppressing parathyroid hormone, which works against vitamin D's efforts to improve bone health by absorbing calcium, they reported.
While heart disease is the leading cause of death in the United States, according to the Centers for Disease Control and Prevention, blacks have higher rates of cardiovascular disease and death than whites and the disease tends to occur earlier in life. The authors write that arterial stiffness and vitamin D deficiency might be potential contributors.
While just how vitamin D is good for our arteries isn't completely understood, it appears to impact blood vessel health in many ways. Laboratory studies have shown that mice missing a vitamin D receptor have higher activation of the renin-angiotensin-aldosterone system, says Raed. Activation of this system increases blood vessel constriction, which can contribute to arterial stiffness. Vitamin D also can suppress vascular smooth muscle cell proliferation, activation of garbage-eating macrophages and calcification formation, all of which can thicken blood vessel walls and hinder flexibility. Vitamin D also reduces inflammation, an underlying mechanism for obesity related development of coronary artery disease, says Raed.
Now it's time to do a larger-scale study, particularly in high-risk populations, and follow participants' progress for longer periods, Dong and Raed say. "A year would give us even more data and ideas," Raed adds.
Dong notes that pulse wave velocity and blood pressure measures are complementary but not interchangeable. "We think maybe in the future, when you go to your physician, he or she might check your arterial stiffness as another indicator of how healthy you are," Raed says.
There were no measurable differences in weight or blood pressure measurements over the 16-week study period.
The Institute of Medicine currently recommends a daily intake of 800 IUs of vitamin D for those age 70 and older. For adolescents and adults, they recommend 4,000 IUs as the upper daily limit; 2,000 was a previous upper limit.
More than 80 percent of Americans, the majority of whom spend their days indoors, have vitamin D insufficiency or deficiency. Dong, an expert in vitamin D and a professor in the MCG Department of Population Health Sciences, says about 15 minutes daily in the "young" sun -- between 10 a.m. and 2 p.m. -- but before your skin starts to get pink, is the best source of vitamin D.
Foods like milk, milk products like cheese and yogurt, fatty fish like mackerel and sardines, some greens like kale and collards and fortified cereals also are good sources. The researchers say a vitamin D supplement is an inexpensive and safe option for most of us.
Story Source:
Materials provided by Medical College of Georgia at Augusta University. Original written by Toni Baker. Note: Content may be edited for style and length.
Journal Reference:
Anas Raed, Jigar Bhagatwala, Haidong Zhu, Norman K. Pollock, Samip J. Parikh, Ying Huang, Robyn Havens, Ishita Kotak, De-Huang Guo, Yanbin Dong. Dose responses of vitamin D3 supplementation on arterial stiffness in overweight African Americans with vitamin D deficiency: A placebo controlled randomized trial. PLOS ONE, 2017; 12 (12): e0188424 DOI: 10.1371/journal.pone.0188424
Cite This Page:
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APA
Chicago
Medical College of Georgia at Augusta University. "High doses of vitamin D rapidly reduce arterial stiffness in overweight/obese, vitamin-deficient African-Americans." ScienceDaily. ScienceDaily, 2 January 2018. <www.sciencedaily.com/releases/2018/01/180102114147.htm>.
Caffeine level in blood may help diagnose people with Parkinson's disease
Date: January 6, 2018 Source: American Academy of Neurology Summary: Testing the level of caffeine in the blood may provide a simple way to aid the diagnosis of Parkinson's disease, according to a new study.
Testing the level of caffeine in the blood may provide a simple way to aid the diagnosis of Parkinson's disease, according to a study published in the January 3, 2018, online issue of Neurology®, the medical journal of the American Academy of Neurology.
The study found that people with Parkinson's disease had significantly lower levels of caffeine in their blood than people without the disease, even if they consumed the same amount of caffeine.
"Previous studies have shown a link between caffeine and a lower risk of developing Parkinson's disease, but we haven't known much about how caffeine metabolizes within the people with the disease," said study author Shinji Saiki, MD, PhD, of Juntendo University School of Medicine in Tokyo, Japan.
People in the study with more severe stages of the disease did not have lower levels of caffeine in the blood, suggesting that the decrease occurs from the earliest stages of the disease, according to David G. Munoz, MD, of the University of Toronto in Canada, who wrote an editorial accompanying the study.
"If these results can be confirmed, they would point to an easy test for early diagnosis of Parkinson's, possibly even before symptoms are appearing," Munoz said. "This is important because Parkinson's disease is difficult to diagnose, especially at the early stages."
The study involved 108 people who had Parkinson's disease for an average of about six years and 31 people of the same age who did not have the disease. Their blood was tested for caffeine and for 11 byproducts the body makes as it metabolizes caffeine. They were also tested for mutations in genes that can affect caffeine metabolism.
The two groups consumed about the same amount of caffeine, with an average equivalent to about two cups of coffee per day. But the people with Parkinson's disease had significantly lower blood levels of caffeine and nine of the 11 byproducts of caffeine in the blood. The caffeine level was an average of 79 picomoles per 10 microliters for people without Parkinson's disease, compared to 24 picomoles per 10 microliters for people with the disease. For one of the byproducts, the level was below the amount that could be detected in more than 50 percent of the people with Parkinson's disease.
In the statistical analysis, the researchers found that the test could be used to reliably identify the people with Parkinson's disease, with a score of 0.98 where a score of 1 means that all cases are identified correctly.
In the genetic analysis, there were no differences in the caffeine-related genes between the two groups.
Limitations of the study include that people with severe Parkinson's disease were not included, which could affect the ability to detect an association between disease severity and caffeine levels. Munoz also noted that all of the people with Parkinson's were taking Parkinson's medication and it's possible that these drugs could affect the metabolism of caffeine.
Story Source:
Materials provided by American Academy of Neurology. Note: Content may be edited for style and length.
Journal Reference:
Motoki Fujimaki, Shinji Saiki, Yuanzhe Li, Naoko Kaga, Hikari Taka, Taku Hatano, Kei-Ichi Ishikawa, Yutaka Oji, Akio Mori, Ayami Okuzumi, Takahiro Koinuma, Shin-Ichi Ueno, Yoko Imamichi, Takashi Ueno, Yoshiki Miura, Manabu Funayama, Nobutaka Hattori. Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease. Neurology, 2018; 10.1212/WNL.0000000000004888 DOI: 10.1212/WNL.0000000000004888
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American Academy of Neurology. "Caffeine level in blood may help diagnose people with Parkinson's disease." ScienceDaily. ScienceDaily, 6 January 2018. <www.sciencedaily.com/releases/2018/01/180106185435.htm>.
Unusual plant immune response to bacterial infection characterized
Date: January 8, 2018 Source: Salk Institute Summary: When you see brown spots on otherwise healthy green leaves, you may be witnessing a plant's immune response as it tries to keep a bacterial infection from spreading. Some plants are more resistant to such infections than others, and plant biologists want to understand why. Scientists studying a plant protein called SOBER1 recently discovered one mechanism by which, counterintuitively, plants seem to render themselves less resistant to infection.
This cartoon depicts a leaf with areas of damage (brown spots) caused by the plant's innate immune response. The superimposed schematic shows SOBER1's three-dimensional structure.
Credit: Salk Institute
When you see brown spots on otherwise healthy green leaves, you may be witnessing a plant's immune response as it tries to keep a bacterial infection from spreading. Some plants are more resistant to such infections than others, and plant biologists want to understand why. Salk Institute scientists studying a plant protein called SOBER1 recently discovered one mechanism by which, counterintuitively, plants seem to render themselves less resistant to infection.
The work, which appeared in Nature Communications on December 19, 2017, sheds light on plant resistance generally and could lead to strategies to boost plants' natural immunity or to better contain infections that threaten to destroy an entire agricultural crop.
"There are a lot of losses in crop yields due to bacteria that kill plants," says the paper's senior author Joanne Chory, a Howard Hughes Medical Institute Investigator, director of Salk's Plant Molecular and Cellular Biology Laboratory and a 2018 recipient of the Breakthrough Prize in Life Sciences. "With this work, we set out to understand the underlying mechanism of how resistance works, and to see how general it is."
One of the ways plants fight bacterial infection is by killing off their own cells in which bacterial proteins are detected. But some bacteria have evolved a counter strategy -- injecting special proteins that suppress the plant's immune response by adding small, disabling chemical tags called acetyl groups to immune molecules. This process is called acetylation. What makes certain plants able to resist these bacterial counter measures while others succumb to infection remains unclear.
As a means to better understand such pathogen-plant interactions, Chory's team turned to the well-studied weed Arabidopsis thaliana and, in particular, an enzyme called SOBER1 -- which had previously been reported to suppress the weed's immune response to a bacterial protein known as AvrBsT. While it may seem counterintuitive to use immune suppression to study infection resistance, the Salk biologists thought doing so could yield useful information.
The researchers started by determining SOBER1's amino acid sequence -- the particular order of building blocks that gives a protein its basic identity. Intriguingly, they found it was very similar to a cancer-pathway-related human enzyme. This enzyme contains a characteristic tunnel into which proteins with certain types of modifications can fit and be cut as part of the enzymatic reaction. It turns out SOBER1 can be classified as part of a vast protein superfamily known as alpha/beta hydrolases. These enzymes share a common core structure but are very flexible in the chemical reactions they catalyze, which range from the breakdown of fat to the detoxification of chemicals called peroxides.
Next, they used a more than 100-year-old technique called X-ray crystallography to determine SOBER1's three-dimensional structure. While similar to the human enzyme, the plant enzyme's tunnel had two extra amino acids sticking down from the top: one at the entrance and one in the middle.
"When we saw those, we realized they had to have a dramatic effect on function because they basically block the tunnel," says Salk research associate and co-first author Marco Bürger.
To discover what the purpose might be, Bürger and co-first author Björn Willige, also a research associate, used substrates (molecules that enzymes act on) with different lengths and biochemically tested how well they fit in the enzyme and whether they could be cut. Only certain types fit and were cut -- very short acetyl groups. This suggested that SOBER1 is a deacetylase -- a class of enzyme that removes acetyl groups. Furthermore, the team mutated SOBER1 and thus opened the blocked tunnel. With this change, Bürger and Willige engineered an enzyme that lost its strong specificity for short acetyl groups and instead preferred longer substrates.
"For the initial biochemistry experiments, we used established, artificial substrates," says Willige. "But next we wanted to see what would happen in plants."
For this, they used tobacco plants -- which have large leaves that are easy to work with -- and a bacterium that makes AvrBsT, which is known to trigger acetylation. They produced AvrBsT in different regions of tobacco leaves along with SOBER1 and several mutated (and thus nonfunctional) versions of the enzyme.
Leaves producing AvrBsT had brown patches of dead tissue, indicating that AvrBsT had initiated a cell death program to curtail the systemic spreading of the pathogen. Leaves that produced AvrBsT together with SOBER1 looked healthy, indicating that SOBER1 reversed the action of AvrBsT. Strikingly, mutated SOBER1 versions with an opened tunnel were not able to prevent the tissue from dying. From this, the researchers concluded that deacetylation must be the underlying chemical reaction leading to suppression of the plant's immune response.
The tobacco tests supported the idea of SOBER1 being a deacetylase that would remove acetyl groups added by bacterial proteins. Without the acetyl groups tagging proteins, the plant didn't recognize them as foreign and thus didn't mount a cell-killing immune response. The leaves looked healthier because cells weren't dying.
"SOBER1's function is surprising because it keeps infected tissue alive, which puts the plant at risk," says Chory, who also holds the Howard H. and Maryam R. Newman Chair in Plant Biology at Salk. "But we are just beginning to understand these types of mechanisms, and there could very well be conditions in which the actions of SOBER1 is beneficial."
Further tests showed that the activity and function of SOBER1 is not restricted to the weed Arabidopsis thaliana, but also exists in a plant called oilseed rape demonstrating that the findings of Chory's lab could be applied to agricultural crops and biofuel resources.
Bürger and Willige would next like to begin screening for chemical inhibitors that could block SOBER1, thereby allowing plants to have a full immune response to pathogenic bacteria.
Story Source:
Materials provided by Salk Institute. Note: Content may be edited for style and length.
Journal Reference:
Marco Bürger, Björn C. Willige, Joanne Chory. A hydrophobic anchor mechanism defines a deacetylase family that suppresses host response against YopJ effectors. Nature Communications, 2017; 8 (1) DOI: 10.1038/s41467-017-02347-w
Cite This Page:
MLA
APA
Chicago
Salk Institute. "Unusual plant immune response to bacterial infection characterized." ScienceDaily. ScienceDaily, 8 January 2018. <www.sciencedaily.com/releases/2018/01/180108130201.htm>.
This cartoon depicts a leaf with areas of damage (brown spots) caused by the plant's innate immune response. The superimposed schematic shows SOBER1's three-dimensional structure.
Credit: Salk Institute
When you see brown spots on otherwise healthy green leaves, you may be witnessing a plant's immune response as it tries to keep a bacterial infection from spreading. Some plants are more resistant to such infections than others, and plant biologists want to understand why. Salk Institute scientists studying a plant protein called SOBER1 recently discovered one mechanism by which, counterintuitively, plants seem to render themselves less resistant to infection.
The work, which appeared in Nature Communications on December 19, 2017, sheds light on plant resistance generally and could lead to strategies to boost plants' natural immunity or to better contain infections that threaten to destroy an entire agricultural crop.
"There are a lot of losses in crop yields due to bacteria that kill plants," says the paper's senior author Joanne Chory, a Howard Hughes Medical Institute Investigator, director of Salk's Plant Molecular and Cellular Biology Laboratory and a 2018 recipient of the Breakthrough Prize in Life Sciences. "With this work, we set out to understand the underlying mechanism of how resistance works, and to see how general it is."
One of the ways plants fight bacterial infection is by killing off their own cells in which bacterial proteins are detected. But some bacteria have evolved a counter strategy -- injecting special proteins that suppress the plant's immune response by adding small, disabling chemical tags called acetyl groups to immune molecules. This process is called acetylation. What makes certain plants able to resist these bacterial counter measures while others succumb to infection remains unclear.
As a means to better understand such pathogen-plant interactions, Chory's team turned to the well-studied weed Arabidopsis thaliana and, in particular, an enzyme called SOBER1 -- which had previously been reported to suppress the weed's immune response to a bacterial protein known as AvrBsT. While it may seem counterintuitive to use immune suppression to study infection resistance, the Salk biologists thought doing so could yield useful information.
The researchers started by determining SOBER1's amino acid sequence -- the particular order of building blocks that gives a protein its basic identity. Intriguingly, they found it was very similar to a cancer-pathway-related human enzyme. This enzyme contains a characteristic tunnel into which proteins with certain types of modifications can fit and be cut as part of the enzymatic reaction. It turns out SOBER1 can be classified as part of a vast protein superfamily known as alpha/beta hydrolases. These enzymes share a common core structure but are very flexible in the chemical reactions they catalyze, which range from the breakdown of fat to the detoxification of chemicals called peroxides.
Next, they used a more than 100-year-old technique called X-ray crystallography to determine SOBER1's three-dimensional structure. While similar to the human enzyme, the plant enzyme's tunnel had two extra amino acids sticking down from the top: one at the entrance and one in the middle.
"When we saw those, we realized they had to have a dramatic effect on function because they basically block the tunnel," says Salk research associate and co-first author Marco Bürger.
To discover what the purpose might be, Bürger and co-first author Björn Willige, also a research associate, used substrates (molecules that enzymes act on) with different lengths and biochemically tested how well they fit in the enzyme and whether they could be cut. Only certain types fit and were cut -- very short acetyl groups. This suggested that SOBER1 is a deacetylase -- a class of enzyme that removes acetyl groups. Furthermore, the team mutated SOBER1 and thus opened the blocked tunnel. With this change, Bürger and Willige engineered an enzyme that lost its strong specificity for short acetyl groups and instead preferred longer substrates.
"For the initial biochemistry experiments, we used established, artificial substrates," says Willige. "But next we wanted to see what would happen in plants."
For this, they used tobacco plants -- which have large leaves that are easy to work with -- and a bacterium that makes AvrBsT, which is known to trigger acetylation. They produced AvrBsT in different regions of tobacco leaves along with SOBER1 and several mutated (and thus nonfunctional) versions of the enzyme.
Leaves producing AvrBsT had brown patches of dead tissue, indicating that AvrBsT had initiated a cell death program to curtail the systemic spreading of the pathogen. Leaves that produced AvrBsT together with SOBER1 looked healthy, indicating that SOBER1 reversed the action of AvrBsT. Strikingly, mutated SOBER1 versions with an opened tunnel were not able to prevent the tissue from dying. From this, the researchers concluded that deacetylation must be the underlying chemical reaction leading to suppression of the plant's immune response.
The tobacco tests supported the idea of SOBER1 being a deacetylase that would remove acetyl groups added by bacterial proteins. Without the acetyl groups tagging proteins, the plant didn't recognize them as foreign and thus didn't mount a cell-killing immune response. The leaves looked healthier because cells weren't dying.
"SOBER1's function is surprising because it keeps infected tissue alive, which puts the plant at risk," says Chory, who also holds the Howard H. and Maryam R. Newman Chair in Plant Biology at Salk. "But we are just beginning to understand these types of mechanisms, and there could very well be conditions in which the actions of SOBER1 is beneficial."
Further tests showed that the activity and function of SOBER1 is not restricted to the weed Arabidopsis thaliana, but also exists in a plant called oilseed rape demonstrating that the findings of Chory's lab could be applied to agricultural crops and biofuel resources.
Bürger and Willige would next like to begin screening for chemical inhibitors that could block SOBER1, thereby allowing plants to have a full immune response to pathogenic bacteria.
Story Source:
Materials provided by Salk Institute. Note: Content may be edited for style and length.
Journal Reference:
Marco Bürger, Björn C. Willige, Joanne Chory. A hydrophobic anchor mechanism defines a deacetylase family that suppresses host response against YopJ effectors. Nature Communications, 2017; 8 (1) DOI: 10.1038/s41467-017-02347-w
Cite This Page:
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Salk Institute. "Unusual plant immune response to bacterial infection characterized." ScienceDaily. ScienceDaily, 8 January 2018. <www.sciencedaily.com/releases/2018/01/180108130201.htm>.
A botanical mystery solved by phylogenetic testing
Date: January 8, 2018 Source: Missouri Botanical Garden Summary: Researchers used DNA testing to rediscover Dracaena umbraculifera, which was thought to be extinct
Missouri Botanical Garden researchers used DNA testing to rediscover Dracaena umbraculifera, which was thought to be extinct. The methods and results were published in Oryx. The authors include Garden researchers in both St. Louis and Madagascar.
Dracaena umbraculifera was described in 1797 from a cultivated plant attributed to Mauritius. However, repeated attempts to locate the plant in Mauritius were unsuccessful. As a result, it was categorized as Extinct on the International Union for Conservation of Nature (IUCN) Red List. There were a number of individuals labeled as D. umbraculifera growing in botanical gardens around the world including the Missouri Botanical Garden. This suggested the status might be inaccurate and that Extinct in the Wild was the correct categorization.
The goal of the authors was to understand where D. umbraculifera actually originated, which species are its close relatives, if it was truly extinct, and to clarify the identity of the individuals growing in botanical gardens. DNA testing indicated D. umbraculifera is more closely related to Dracaena reflexa from Madagascar than to Mauritian Dracaena. Armed with that information, a number of the authors conducted field expeditions in Madagascar, ultimately discovering five wild populations. They concluded that the species' IUCN status should be critically endangered rather than extinct.
This study highlights the importance of living collections in botanical gardens, even those that are centuries old and might lack information about origin. The genetic analysis of these plants can play an important role in making new discoveries particularly about poorly known species. D. umbraculifera, for example, was likely overlooked by botanists during field work because its origin was assumed to be Mauritius rather than Madagascar. The findings further confirm the importance of additional work in the flora-rich Madagascar and other islands of the western Indian Ocean. Nearly 90 percent of plants in this region are endemic, but are threatened due to ongoing deforestation. There is an urgent need to document and conserve this biodiversity.
Dr. Christine Edwards, Dr. Burgund Bassuner, Dr. Porter Lowry, Senior Vice President Dr. James Miller, Senior Vice President Andrew Wyatt and Garden President Dr. Peter Wyse Jackson, Dr. Chris Birkinshaw, Christian Camara and Adolphe Lehavana served as authors.
"This project is a great example of how DNA analysis can be used to both bring new value to botanical garden collections and to make new discoveries. It is particularly exciting because it is rare to have the opportunity to rediscover a species that hasn't been seen in the wild for 200 years," said Edwards.
Story Source:
Materials provided by Missouri Botanical Garden. Note: Content may be edited for style and length.
Journal Reference:
Christine E. Edwards, Burgund Bassüner, Chris Birkinshaw, Christian Camara, Adolphe Lehavana, Porter P. Lowry, James S. Miller, Andrew Wyatt, Peter Wyse Jackson. A botanical mystery solved by phylogenetic analysis of botanical garden collections: the rediscovery of the presumed-extinct Dracaena umbraculifera. Oryx, 2018; 1 DOI: 10.1017/S0030605317001570
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Missouri Botanical Garden. "A botanical mystery solved by phylogenetic testing." ScienceDaily. ScienceDaily, 8 January 2018. <www.sciencedaily.com/releases/2018/01/180108090235.htm>
Missouri Botanical Garden researchers used DNA testing to rediscover Dracaena umbraculifera, which was thought to be extinct. The methods and results were published in Oryx. The authors include Garden researchers in both St. Louis and Madagascar.
Dracaena umbraculifera was described in 1797 from a cultivated plant attributed to Mauritius. However, repeated attempts to locate the plant in Mauritius were unsuccessful. As a result, it was categorized as Extinct on the International Union for Conservation of Nature (IUCN) Red List. There were a number of individuals labeled as D. umbraculifera growing in botanical gardens around the world including the Missouri Botanical Garden. This suggested the status might be inaccurate and that Extinct in the Wild was the correct categorization.
The goal of the authors was to understand where D. umbraculifera actually originated, which species are its close relatives, if it was truly extinct, and to clarify the identity of the individuals growing in botanical gardens. DNA testing indicated D. umbraculifera is more closely related to Dracaena reflexa from Madagascar than to Mauritian Dracaena. Armed with that information, a number of the authors conducted field expeditions in Madagascar, ultimately discovering five wild populations. They concluded that the species' IUCN status should be critically endangered rather than extinct.
This study highlights the importance of living collections in botanical gardens, even those that are centuries old and might lack information about origin. The genetic analysis of these plants can play an important role in making new discoveries particularly about poorly known species. D. umbraculifera, for example, was likely overlooked by botanists during field work because its origin was assumed to be Mauritius rather than Madagascar. The findings further confirm the importance of additional work in the flora-rich Madagascar and other islands of the western Indian Ocean. Nearly 90 percent of plants in this region are endemic, but are threatened due to ongoing deforestation. There is an urgent need to document and conserve this biodiversity.
Dr. Christine Edwards, Dr. Burgund Bassuner, Dr. Porter Lowry, Senior Vice President Dr. James Miller, Senior Vice President Andrew Wyatt and Garden President Dr. Peter Wyse Jackson, Dr. Chris Birkinshaw, Christian Camara and Adolphe Lehavana served as authors.
"This project is a great example of how DNA analysis can be used to both bring new value to botanical garden collections and to make new discoveries. It is particularly exciting because it is rare to have the opportunity to rediscover a species that hasn't been seen in the wild for 200 years," said Edwards.
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Materials provided by Missouri Botanical Garden. Note: Content may be edited for style and length.
Journal Reference:
Christine E. Edwards, Burgund Bassüner, Chris Birkinshaw, Christian Camara, Adolphe Lehavana, Porter P. Lowry, James S. Miller, Andrew Wyatt, Peter Wyse Jackson. A botanical mystery solved by phylogenetic analysis of botanical garden collections: the rediscovery of the presumed-extinct Dracaena umbraculifera. Oryx, 2018; 1 DOI: 10.1017/S0030605317001570
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Missouri Botanical Garden. "A botanical mystery solved by phylogenetic testing." ScienceDaily. ScienceDaily, 8 January 2018. <www.sciencedaily.com/releases/2018/01/180108090235.htm>
segunda-feira, 26 de março de 2018
domingo, 25 de março de 2018
Usos e curiosidades sobre as plantas espontâneas. Maria-pretinha
Texto:
- Giovanna Brito Lins - Graduanda em Ciência e Tecnologia e Ciências Biológicas na Universidade Federal do ABC
- Marcos Roberto Furlan - Engenheiro Agrônomo - Professor - Faculdade Cantareira/Unitau
Originária do continente americano, a maria-pretinha (Solanum americanum), de aparência delicada, pertence à família Solanaceae. Produz pequenas flores brancas. Seus frutos, quando maduros, apresentam-se pretos e suas folhas exalam cheiro pouco atrativo
A família Solanaceae é composta por vários outros representantes muito conhecidos e consumidos, como, por exemplo, batata-inglesa, berinjela, jiló, tomate e pimentas do gênero Capsicum. Muitas solanáceas possuem folhas ou frutos tóxicos, devido a substâncias como a solanina e outros alcaloides. As folhas da maria-pretinha não são comestíveis cruas, pois podem causar complicações gastrointestinais. Salvo as folhas, os frutos apresentam eficácia medicinal comprovada, além de várias outras aplicações.
A maria-pretinha é, ainda, conhecida popularmente como erva-moura, erva-moura-açu, caraxixu, pimenta-de-bugre, dentre outros nomes. É válido ressaltar que é de suma importância atentar-se ao nome científico da espécie utilizada, uma vez que há outra espécie também chamada de erva-moura e semelhante à Solanum americanum. É a Solanum nigrum, conhecida também por "mata-cavalo" devido a tamanha toxicidade dos frutos quando consumidos crus.
Solanum americanum
10 usos e curiosidades sobre a maria-pretinha
1. A ocorrência da maria-pretinha nos campos, quintais ou na horta, pode servir para obter algumas informações relacionadas ao cultivo. Sua presença, caso verifique a incidência de viroses, pode ser um recado para que evite o plantio de hortaliças da família Solanaceae. Também é comum ser atacada por pulgões, dentre outras pragas que também atacam hortaliças.
2. Na medicina popular, a planta é utilizada como diurética, laxante, emoliente, além de eliminar toxinas e resíduos do organismo. É de uso bastante comum principalmente em rincões nas zonas rurais do país. O chá das, em específico, é usado para aliviar nervosismo, cólicas, reumatismo, artrite, nevralgia, ferimentos, afecções das vias urinárias, espasmos na bexiga, dores musculares, no estômago, articulações e na coluna, psoríase, eczema, úlceras, contusões, hidropsia; além de ser um ótimo vermífugo natural.
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3. É considerada a "blueberry brasileira" por alguns autores. Sendo fácil encontrar receitas de geleias, compotas, sucos, chás, bolos, sorvetes, mousses e panquecas.
4. Algumas religiões Afro-brasileiras a utilizam em banhos de limpeza (amacis e abôs), lavagem de contas, sacudimentos, bate-folhas e oferendas;
5. O nome do gênero diz respeito à palavra "Solamen" do Latim, o qual pode ser traduzido como "quietude" ou "alívio'' em alusão às propriedades calmantes ou mesmo narcóticas de alguns espécimes. O epíteto específico "americanum" deve-se à origem continental da espécie.
6. Abaixo, de acordo com Ranieri, G. 2016, seguem-se as formas de se distinguir, visualmente, a Solanum americanum e Solanum nigrum:
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7. Kinnup (2010) ressalta que a etnia Kaingang, localizada no sul do Brasil, consome esta espécie cozida utilizando-se do nome "fuá" e, inclusive, há relatos de grandes colheitas da planta no interior do Rio Grande do Sul realizadas pelos indígenas.
8. China, Guatemala, África do Sul e El Salvador são exemplos de países onde também se consome a Solanum americanum com regularidade e, no caso das folhas, sempre cozidas;
9. É considerada rica em proteínas, manganês (Mn), fósforo (P), ferro (Fe) e boro (B).
10. Os frutos de coloração escura evidenciam a presença de antocianinas, intimamente relacionadas à potenciais aplicações enquanto antioxidante.
Referências
Etimologia:
Kinnup, V. F., Plantas alimentícias não-convencionais da região metropolitana de Porto Alegre, RS.
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