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Target Health Closed Between December 25 and January 3

Continuing our tradition of giving our loyal and dedicated staff more time with their families over the holiday season, Target Health will again be closed between December 25, 2009 and January 1, 2010, with all back to work on January 4, 2010.  Since we always have ongoing business, even during holidays all key employees will be available via email or cell phone for all urgent matters. The EDC Help Desk will still be operating 24/7.

For more information about Target Health and our software tools for paperless clinical trials, please contact Dr. Jules T. Mitchel (212-681-2100 ext 0) or Ms. Joyce Hays. Target Health’s software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website at: www.targethealth.com

Taste Develops in Utero

Most of us assume that the womb is like Grandma’s off-limits closet: dark and mysterious. But the truth is that there is some connection to the outside 1) ___ while a baby is in utero, and that many people develop preferences based on experiences during those 9 months. Here’s what developed when you first started to smell and 2) ___. Scientists used to believe that fetuses had no sense of 3) ___. We now know that, before birth, amniotic fluid moves through the nasal and oral cavities, and that develops sense of smell — an ability that starts at about 30 weeks. Taste buds start to develop in utero by week 8, and they begin communicating with the 4) ___ about 5 weeks later. Located around the perimeter of the tongue, each of the 4,500 taste buds has about 40 receptor cells, which bind with food and send information to the brain. A 5) ___ can taste some flavors by 8 weeks, and by 15 to 17 weeks, the amniotic fluid can taste of curry, cumin, onion, or other foods from the mother’s diet. The taste of the 6) ___ ___ changes all the time, depending on what mother is eating, which may strongly influence what the baby will prefer later in life. Abstracted from Mehmet Oz, MD and, Michael Roizen, MD

ANSWERS: 1) world; 2) taste; 3) smell; 4) brain; 5) fetus; 6) amniotic fluid 

Diabetes

Ancient Hindu writings, many thousands of years old, document how black ants and flies were attracted to the urine of diabetics. The Indian physician Sushruta in 400 BCE described the sweet taste of urine from affected individuals, and for many centuries to come, the sweet taste of urine was key to the diagnosis of diabetes. Around 250 BCE, the name “diabetes” was first used. It is a Greek word that means “to syphon”, reflecting how diabetes seemed to rapidly drain fluid from the affected individual. The Greek physician Aretaeus noted that as affected individuals wasted away, they passed increasing amounts of urine as if there was “liquefaction of flesh and bones into urine”. The complete term “diabetes mellitus” was coined in 1674 by Thomas Willis, personal physician to King Charles II. Mellitus is Latin for honey, which is how Willis described the urine of diabetics (“as if imbued with honey and sugar”). Up until the mid-1800s, the treatments offered for diabetes varied tremendously. Various “fad” diets were prescribed, and the use of opium was suggested, as were bleeding and other therapies. The most successful treatments were starvation diets in which calorie intake was severely restricted. Naturally, this was intolerable for the patient and at best extended life expectancy for a few years. A breakthrough in the puzzle of diabetes came in 1889 when German physicians Joseph von Mering and Oskar Minkowski surgically removed the pancreas from dogs. The dogs immediately developed diabetes. As the link was established between the pancreas gland and diabetes, research focused on isolating the pancreatic extract that could treat diabetes. When Dr. Frederick Banting took up the challenge of isolating a pancreatic extract, he was met with much skepticism. But Banting, a surgeon, persisted and in May 1921, he began work in the laboratory of Professor John Macloed in Toronto, Canada. Charles Best, a medical student at the time, worked as his assistant. To concentrate what we now know as insulin, Banting tied the pancreatic ducts of dogs. The pancreatic cells that released digestive enzymes (and could also destroy insulin) degenerated, but the cells that secreted insulin were spared. Over several weeks the pancreas degenerated into a residue from which insulin could be extracted. In July 1921, a dog that had had its pancreas surgically removed was injected with an extract collected from a duct-tied dog. In the two hours that followed the injection, the blood sugar level of the dog fell, and its condition improved. Another de-pancreatized (diabetic-like) dog was kept alive for eight days by regular injections until supplies of the extract, at that time called “isletin”, were exhausted. Further experiments on dogs showed that extracts from the pancreas caused a drop in blood sugar, caused glucose in the urine to disappear, and produced a marked improvement in clinical condition. So long as the extract was being given, the dogs were kept alive. The supply of the extract was improved: the pancreas of different animals were used until that of the cow was settled upon. This extract kept a de-pancreatized dog alive for 70 days. Dr. James B. Collip, a biochemist, was drafted to continue improving the purity of the pancreas extract, and later, Best carried on this work. A young boy, Leonard Thompson, was the first patient to receive insulin treatment. On January 11, 1922, aged 14 and weighing only 64 pounds, he was extremely ill. The first injections of insulin only produced a slight lowering of blood sugar level. The extract still was not pure enough, and abscesses developed at the injection site. Collip continued to refine the extract. Several weeks later, Leonard was treated again and showed a remarkable recovery. His blood sugar levels fell, he gained weight and lived for another 13 years. He died from pneumonia at the age of 27. During the spring of 1922, Best increased the production of insulin to enable the treatment of diabetic patients coming to the Toronto clinic. Over the next 60 years, insulin was further refined and purified, and long-acting and intermediate types were developed to provide more flexibility. A revolution came with the production of recombinant human DNA insulin in 1978. Instead of collecting insulin from animals, new human insulin could be synthesized. In 1923, Banting and Macloed were awarded the Nobel Prize for the discovery of insulin. Banting split his prize with Best, and Macloed split his prize with Collip. In his Nobel Lecture, Banting concluded the following about their discovery: “Insulin is not a cure for diabetes; it is a treatment. It enables the diabetic to burn sufficient carbohydrates, so that proteins and fats may be added to the diet in sufficient quantities to provide energy for the economic burdens of life.”

Novel Antibody Associated with Autoimmune Pancreatitis

Autoimmune pancreatitis is characterized by an inflammatory process that leads to organ dysfunction. The cause of the disease is unknown, and while its autoimmune origin has been suggested it has never been proved. In addition, little is known about the pathogenesis of this condition. As a result, a study published in the New England Journal of Medicine (2009;361:2135-2142), was performed to identify pathogenetically relevant autoantigen targets from a random peptide library with pooled IgG obtained from 20 patients with autoimmune pancreatitis. Results showed that peptide-specific antibodies were detected in serum specimens obtained from the patients. Among the detected peptides, peptide AIP1-7 was recognized by the serum specimens from 18 of 20 patients with autoimmune pancreatitis and by serum specimens from 4 of 40 patients with pancreatic cancer, but not by serum specimens from healthy controls. The peptide showed homology with an amino acid sequence of plasminogen-binding protein (PBP) of Helicobacter pylori and with ubiquitin-protein ligase E3 component n-recognin 2 (UBR2), an enzyme highly expressed in acinar cells of the pancreas. Antibodies against the PBP peptide were detected in 19 of 20 patients with autoimmune pancreatitis (95%) and in 4 of 40 patients with pancreatic cancer (10%). Such reactivity was not detected in patients with alcohol-induced chronic pancreatitis or intraductal papillary mucinous neoplasm. The results were validated in another series of patients with autoimmune pancreatitis or pancreatic cancer: 14 of 15 patients with autoimmune pancreatitis (93%) and 1 of 70 patients with pancreatic cancer (1%) had a positive test for anti-PBP peptide antibodies. When the training and validation groups were combined, the test was positive in 33 of 35 patients with autoimmune pancreatitis (94%) and in 5 of 110 patients with pancreatic cancer (5%).

Can Association Between Preterm Birth and Autism be Explained by Maternal or Neonatal Morbidity?

A study reported in Pediatrics (2009;124: e817-e825) was performed to examine whether an association between preterm birth and risk of autistic disorders could be explained by pregnancy complications or neonatal morbidity. This Swedish, population-based, case-control study included 1,216 case subjects with autistic disorders who were born between 1987 and 2002 and 6,080 control subjects who were matched with respect to gender, birth year, and birth hospital. Associations were assessed between gestational age and autistic disorders and adjusted for maternal, birth, and neonatal characteristics. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Results showed that compared with infants born at term, the unadjusted ORs for autistic disorders among very and moderately preterm infants were 2.05 and 1.55, respectively. When maternal, pregnancy and birth characteristics were controlled for, ORs were reduced to 1.48 and 1.33, respectively. When neonatal complications were controlled for, ORs were 0.98 and 1.25, respectively. Reductions in risks of autistic disorders related to preterm birth were primarily attributable to preeclampsia, small-for-gestational age birth, congenital malformations, low Apgar scores at 5 minutes, and intracranial bleeding, cerebral edema, or seizures in the neonatal period. Neonatal hypoglycemia, respiratory distress, and neonatal jaundice were associated with increased risk of autistic disorders for term but not preterm infants. According to the authors, the increased risk of autistic disorders related to preterm birth is mediated primarily by prenatal and neonatal complications that occur more commonly among preterm infants.

Complete Local Elimination of Infectious Trachoma from Severely Affected Communities after Six Biannual Mass Azithromycin Distributions

Trachoma is the result of infection of the eye with Chlamydia trachomatis. Infection spreads from person to person, and is frequently passed from child to child and from child to mother, especially where there are shortages of water, numerous flies, and crowded living conditions. Infection often begins during infancy or childhood and can become chronic. If left untreated, the infection eventually causes the eyelid to turn inwards, which in turn causes the eyelashes to rub on the eyeball, resulting in intense pain and scarring of the front of the eye. This ultimately leads to irreversible blindness, typically between 30 and 40 years of age. A study published in the journal Ophthalmology (2009; 116:2047-2050), was performed to determine whether infectious trachoma can be completely eliminated from severely affected villages by treatment with azithromycin. The study was a cross-sectional survey of 2 villages in Ethiopia previously enrolled and monitored over 42 months as part of a larger, group-randomized clinical trial. A total of 758 individuals were evaluated who resided in 2 villages with high baseline trachoma prevalence, of a total population of 768 (98.7%). For the study, all members of the 2 villages were offered 6 biannual mass treatments with oral azithromycin. At 42 months, each current village member was examined. The right upper tarsal conjunctiva was everted and swabbed. Samples were processed for evidence of Chlamydia trachomatis RNA. The main outcome measure was clinical activity by World Health Organization simplified grading scale for trachoma and laboratory evidence of chlamydial RNA. Results showed that average antibiotic coverage over the study period was 90% and 94% in the 2 villages. Clinical trachoma activity in children aged 1 to 5 years decreased from 78% and 83% in the 2 villages before treatment to 17% and 24% at 42 months. Polymerase chain reaction (PCR) evidence of infection in the same age group decreased from 48% to 0% in both villages at 42 months. When all age groups were examined, there were zero cases with evidence of chlamydial RNA among 758 total villagers tested. According to the authors, biannual mass distribution of azithromycin can locally eliminate ocular chlamydial infection from severely affected communities.

TARGET HEALTH excels in Regulatory Affairs and works closely with many of its clients performing all FDA submissions. TARGET HEALTH receives daily updates of new developments at FDA. Each week, highlights of what is going on at FDA are shared to assure that new information is expeditiously made available.

Medical Food

The term medical food, as defined in section 5(b) of the Orphan Drug Act (21 U.S.C. 360ee (b) (3)) is “a food which is formulated to be consumed or administered enterally under the supervision of a physician and which is intended for the specific dietary management of a disease or condition for which distinctive nutritional requirements, based on recognized scientific principles, are established by medical evaluation.” The FDA advises that it considers the statutory definition of medical foods to narrowly constrain the types of products that fit within this category of food (see Food Labeling; Reference Daily Intakes and Daily Reference Values; Mandatory Status of Nutrition Labeling and Nutrition Content Revision proposed rule (56 FR 60366 at 60377, November 27, 1991)).

Medical foods are distinguished from the broader category of foods for special dietary use and from foods that make health claims by the requirement that medical foods be intended to meet distinctive nutritional requirements of a disease or condition, used under medical supervision and intended for the specific dietary management of a disease or condition. The term “medical foods” does not pertain to all foods fed to sick patients. Medical foods are foods that are specially formulated and processed (as opposed to a naturally occurring foodstuff used in a natural state) for the patient who is seriously ill or who requires the product as a major treatment modality. In general, to be considered a medical food, a product must, at a minimum, meet the following criteria:

1. the product must be a food for oral or tube feeding;
2. the product must be labeled for the dietary management of a specific medical disorder, disease, or condition for which there are distinctive nutritional requirements;
3. the product must be intended to be used under medical supervision 

The following criteria that clarify the statutory definition of a medical food can be found in the agency’s regulations at 21 CFR 101.9(j) (8). A food is a medical food exempt from nutrition labeling only if:

1. It is a specially formulated and processed product (as opposed to a naturally occurring foodstuff used in its natural state) for the partial or exclusive feeding of a patient by means of oral intake or enteral feeding by tube;
2. It is intended for the dietary management of a patient who, because of therapeutic or chronic medical needs, has limited or impaired capacity to ingest, digest, absorb, or metabolize ordinary foodstuffs or certain nutrients, or who has other special medically determined nutrient requirements, the dietary management of which cannot be achieved by the modification of the normal diet alone;
3. It provides nutritional support specifically modified for the management of the unique nutrient needs that result from the specific disease or condition, as determined by medical evaluation;
4. It is intended to be used under medical supervision; and
5. It is intended only for a patient receiving active and ongoing medical supervision wherein the patient requires medical care on a recurring basis for, among other things, instructions on the use of the medical food.

 

Examples of Medical Foods include:

Folgard RX 2.2®: This medical food is indicated for the management of elevated homocysteine, or hyperhomocysteinemia, associated with cardiovascular disease, stroke, and other diseases. Folgard is a formula containing folic acid, vitamin B6 and vitamin B12, designed to lower plasma homocysteine levels.

Limbrel^TM: This medical food is used in the nutritional management of metabolic processes associated with osteoarthritis. Damaged joints release excess phospholipids, which increase the production of prostaglandins and leukotrienes, leading to an inflammatory response. Limbrel is formulated with naturally occurring ingredients that inhibit the two enzymes lipoxygenase and cycloxygenase responsible for the production of inflammatory irritants.

 

For more information about our expertise in Regulatory Affairs, please contact Dr. Jules T. Mitchel or Dr. Glen Park.

WebMD, November 26, 2009  –  The biggest event of Thanksgiving is preparing the turkey, though competing with watching parades and football games on TV all day, is the preparation of the Thanksgiving meal. Thanksgiving Day is a time-honored American tradition, a time for family gatherings and a holiday meal that encourages over-the-top decadence, according to WebMD.com. And for many (some 97% of us), the thought of a Thanksgiving without turkey is heresy. Americans gobble up roughly 45 million turkeys to celebrate the annual holiday.

Do you know that the average Thanksgiving dinner has over 2000 calories? It can be a real challenge if you are watching your waistline, according to HealthCastle.com. The following are some eating tips so that you can still look good and be healthy after the Thanksgiving dinner without having to deprive yourself. Here are some healthy tips for the day. If you are a guest of a Thanksgiving dinner:
1.) Don’t go to the Thanksgiving dinner hungry: we often eat faster and more when we are hungry – therefore eat a wholesome breakfast and lunch on the day to avoid overeating at dinner time.
2.) Thanksgiving dinner is not an all-you-can-eat buffet: Fill your plate half with vegetables, one quarter with a lean meat and the rest with a starch of your choice. Eat slowly and stop when you are full.
3.) Turkey – go skinless: choose your 4-oz turkey portion skinless to slash away some fat and cholesterol. Save your appetite for the side dishes and desserts.
4.) Side Dishes – watch your portion size: go for smaller portions. This way you can sample all the different foods. Moderation is always the key.
5.) Make a conscious choice to limit high fat items: high fat food items can be found in fried and creamy dishes as well as cheese-filled casseroles in a traditional Thanksgiving meal . For instance, mashed potatoes are usually made with butter and milk; green bean casseroles are often prepared with cream of mushroom soup, cheese and milk and topped with fried onions; candied yams are loaded with cream, sugar and marshmallows. If you cannot control the ingredients that go in to a dish, simply limit yourself to a smaller helping size. Again moderation is the key.
6.) Drink plenty of water: alcohol and coffee can dehydrate your body. Drink calorie-free water to help fill up your stomach and keep you hydrated.

If you are the honorable chef of a Thanksgiving dinner:
1.) Substitute high fat ingredients with lower-fat or fat-free ingredients.
2.) Leftover Turkey? Instead of turkey sandwiches, use the leftover turkey to make a pot of soup with fresh chunky vegetables.
3.) Experiment with new recipes: Do a search on Google for numerous delicious yet healthy low-fat contemporary Thanksgiving recipes. Experiment!

According to WebMD.com, it’s always important to follow safe food handling practices to reduce the risk of food-borne illness. This year, consumers may also be worried about the potential for bird flu in their turkeys. But the U.S. Department of Agriculture (USDA) Food Safety and Inspection Service reassures us that bird flu (avian influenza) is not transmissible by eating poultry. The real concern, as always, is viruses and bacterial contamination. The Mississippi Department of Health (MDH) encourages all holiday cooks to add food safety to their list of necessary kitchen ingredients. In the home or in a restaurant, preparing food involves both health and safety, so please observe the following advice:
1.  Remember to cook turkey to the proper internal temperature of 165 degrees Fahrenheit (°F). –Cook roast, pork, and fish to at least 145 degrees Fahrenheit, ground beef to at least 155 degrees Fahrenheit. Sauces, soups and gravy must come to a boil when reheating.
2.  Do not cross-contaminate, and be sure to cool foods properly. Never place cooked food on a plate which previously held raw meat, poultry or seafood.
3.  Always cook dressing separately from the turkey. Place the dressing in the turkey after both are cooked.
4.  Always wash your hands before and after handling food. Wash your hands with hot soapy water after using the bathroom, changing diapers and handling pets.
5.  Wash surfaces often. Those preparing the meal should wash cutting boards, dishes, utensils and counter tops with hot soapy water after preparing each food item.
6.  Refrigerate or freeze prepared food and leftovers within two hours.
7.  Do not overload your refrigerator: space items loosely so that cool air can circulate.
8.  Divide large amounts of leftovers into small, shallow containers for quick cooling.
9.  Thaw food in the refrigerator, under cold running water, or in the microwave – never defrost food at room temperature.

The National Turkey Federation and USDA suggest following these guidelines — along with using a meat thermometer — when roasting an unstuffed bird:
8-12 pounds: 2 3/4 to 3 hours
12-14 pounds: 3 to 3 3/4 hours
14-18 pounds: 3 3/4 to 4 1/4 hours
18-20 pounds: 4 1/4 to 4 1/2 hours
20-24 pounds: 4 1/2 to 5 hours
As you prepare for your upcoming celebration, keep these safety and preparation tips in mind to make sure you enjoy a happy and healthy holiday.

Super Healthy Foods Are On the List!We expect to see leafy greens, tomatoes and power fruits like berries on the list of “super healthy” foods we should be eating more of…but we are not expecting to see them on the list of the 10 riskiest foods regulated by the U.S. Food And Drug Administration (FDA).

The Center for Science in the Public Interest (CSPI) authored this just-released report and identified which FDA regulated foods are responsible for the most food-borne outbreaks (using data from the Centers for Disease Control and Prevention and elsewhere). The FDA is responsible for regulating 80% of the food supply including produce, seafood, egg & dairy and typical packaged foods such as peanut butter and cookie dough.

Here’s the list with the top three being the heaviest hitters:

1. Leafy greens, involved in 363 outbreaks and 13,568 reported cases of illness.
2. Eggs, involved in 352 outbreaks and 11,163 reported cases of illness.
3. Tuna, involved in 268 outbreaks and 2,341 reported cases of illness.
4. Oysters, involved in 132 outbreaks and 3,409 reported cases of illness.
5. Potatoes, involved in 108 outbreaks and 3,659 reported cases of illness.
6. Cheese, involved in 83 outbreaks and 2,761 reported cases of illness.
7. Ice cream, involved in 74 outbreaks and 2,594 reported cases of illness.
8. Tomatoes, involved in 31 outbreaks and 3,292 reported cases of illness.
9. Sprouts, involved in 31 outbreaks and 2,022 reported cases of illness.
10. Berries, involved in 25 outbreaks and 3,397 reported cases of illness.

Tell me more about the top 3#1 Leafy greens
The majority of the outbreaks were linked to the norovirus, spread by unwashed hands of an ill food handler or consumer. The rest were mostly caused by E. coli and salmonella.

What can you do about it?
Well, since most of the outbreaks occurred in restaurants, we need to choose our restaurants carefully as always. Chlorine washes and other post-harvest treatments can reduce cross contamination but they don’t completely eliminate risk. According to CSPI, most of the leafy greens sold have already been through washing and treatment tanks that are more high tech than we could achieve washing them in our own sink. Although this doesn’t help you when eating a salad, cooking the greens will reduce the risk of contamination because the heat kills the bacteria.

Does organic increase or decrease the risk of food poisoning? The Center for Disease Control doesn’t break out their data on outbreaks based on regular or organic produce, but CSPI is assuming that the risk is similar.

#2 Eggs
The majority of illnesses from eggs can be traced to the “S” word – salmonella. The 1970s saw a big reduction in risk of salmonella from eggs thanks to new regulations for cleaning and inspecting eggs (most types of salmonella live in the intestinal tracts of the birds and when the egg is contaminated with the feces, it can be passed to humans.) But unfortunately it isn’t that simple. Today the most common type of salmonella (salmonella enteriditis) contaminates the eggs before the shells are even formed because this type of Salmonella infects the ovaries of the hens.What can you do about it?
Luckily the future looks brighter for egg lovers. New regulations aimed at minimizing salmonella enteriditis in egg production become effective in 2010 or 2012, depending on the size of the egg producer). As always though, cooking eggs thoroughly destroys most pathogens and serving eggs raw or “runny” or leaving egg dishes near room temperature for too long can encourage bacteria to multiply.

#3 Tuna
Much of the risk here has to do with fresh tuna, not canned, and tuna eaten in restaurants, not at home. The main culprit is a toxin called scombrotoxin that is released when fresh fish is stored above 60 degrees Fahrenheit and begins to decay. Symptoms of scombroid poisoning can include skin flushing, headaches, abdominal cramps, nausea, diarrhea, palpitations and loss of vision. There have been some outbreaks from tuna salad consumption so canned tuna is not completely off the hook (so to speak).What can you do about it?
Adequate refrigeration and handling can slow the process of fish spoiling, according to CSPI, but surprisingly the toxin cannot be destroyed (once released) by cooking, freezing or canning. Eating tuna raw or cooked in restaurants doesn’t seem to make a difference in risk. If buying tuna is your aim (in restaurants or in grocery stores or fish markets) make every effort to choose seafood suppliers that are known for having high standards for their fish and handling practices.

For more information, read the entire report: The 10 Riskiest Foods Regulated By The U.S. Food And Drug Administration.

Fluorescent FT protein in the phloem of an Arabidopsis plant.
Courtesy of Laurent Corbesier and George Coupland

 

Researchers unfold a key step in the process that tells plants to flower, findings that could one day benefit agriculture.

The-Scientist.com, November 23, 2009, by Bob Grant   –  Few acts of nature seem simpler than flowers blooming on the outstretched tips of a plant’s shoots. But the induction of that seemingly simple process baffled plant biologists for almost 60 years.

In the 1930s, Cornell University plant scientist James Knott coined the term “florigen” for a mysterious signal that instructs flowers to begin growing at the tips of stems, called apical meristems.¹ Researchers knew and had demonstrated that changes in day length and temperature caused plants to flower, a process essential to plant reproduction. Knott tracked the unidentified florigen traveling through the vascular system of a spinach plant, and other scientists worked out parts of the molecular pathway that allowed plants to sense environmental changes and respond by producing flowers. But the chemical identity of florigen eluded discovery. “It was a technical challenge to put that last nail in the coffin,” says Richard Amasino, a plant scientist at the University of Wisconsin in Madison.

Then in 2007, researchers at the Max Planck Institute for Plant Breeding Research in Cologne, Germany, cracked the case. Plant geneticist George Coupland and colleagues showed that florigen, at least in the flowering Arabidopsis plants they were studying, was a protein encoded by the gene FLOWERING LOCUS T (FT), which behaves like certain types of kinase inhibitors in plant cells. “People were not expecting [florigen] to be a protein or a nucleic acid,” Coupland recalls. “They were expecting it to be a hormone or small molecule,” which typically act as chemical signals in plants.

“It was very clear that FT was the signal,” says Jorge Dubcovsky, a University of California, Davis, plant geneticist who was not involved with the study. Nailing down the identity of florigen meant that science finally identified all the key molecular puzzle pieces involved in flowering-a process of great interest to agriculturalists, for whom an understanding of the molecular machinery of flowering could lead to greater control of their crops by speeding up or slowing down blossom production. “We’ve got the major mysteries solved,” says Amasino. Since Coupland’s long-awaited discovery, his lab and others have continued to answer other lingering questions in flowering pathways, while other plant biologists have corroborated his results and pinpointed the identity of florigen in other, more agriculturally relevant, plants.

False positive

As Coupland and his group sought to provide support for their hypothesis that florigen was a protein, Swedish researchers in 2005 claimed that they had discovered that florigen was mRNA transcribed from the FT gene.² But the Swedish paper showed an extremely low level of FT mRNA in the meristem, which Coupland says that his group saw as a potential artifact of the real-time PCR method used to detect it. Other researchers shared Coupland’s misgivings. Meanwhile, Science, which published the 2005 paper, was heralding it as a “breakthrough of the year,” and plant biology textbooks began reporting that florigen was FT mRNA.

Coupland and his colleagues continued their experiments, but the 2005 Science paper did cause Coupland to be extra careful about assembling his evidence that the FT protein was florigen. “We couldn’t do exactly the same experiments” as the authors of that paper, such as using PCR to show which molecule was moving from leaves to stem tips to induce flowering, Coupland says.

The Coupland group tagged the FT protein with a fluorescent protein, and using microscopy, showed FT moving from leaves through the phloem-a central vascular tissue that transports water in plants-to the apical meristem, where it induced the growth of Arabidopsis flowers. The researchers also grafted one plant to another and showed that the FT protein was moving from the leaf of one plant to the meristem of the other-further proof that the protein was the long-distance carrier of the flowering signal. They also tracked FT mRNA in these experiments, but failed to find those molecules crossing the junction between the grafted plants.

They submitted their paper to Science; later it came to light that the FT mRNA paper contained serious flaws and was retracted from the journal. The first author on the paper was accused of fudging some crucial data. “There was some fearsome competition there,” says Dubcovsky, “and some people put a priority on speed over certainty.”

Crop confirmation

In the same issue of Science where Coupland published his results, a Japanese team identified an ortholog of the FT protein as the florigen in rice (another Hot Paper).³ William Lucas, a UC Davis plant biologist, confirmed that the FT protein was florigen in pumpkins,⁴ while Dubcovsky identified a florigen protein homologous to FT protein in wheat.⁵ The FT protein has also been shown to induce flowering in poplar trees.⁶

But more mysteries about flowering physiology remain. “[Identifying florigen is] a very important piece of the puzzle, but there’s still a lot to be done,” says Dubcovsky. For example, there is no direct evidence to show how the protein moves through the phloem, according to Coupland. His group is working to characterize some of the mechanistic links between the FT protein and other players in the flowering pathway, such as CONSTANS, a transcriptional regulator that triggers the transcription of FT in leaves and the bZIP transcription factor FD, which interacts with the FT protein to deliver the flower induction signal to its target in the meristem. “There may well be other things to find out in the details of this model,” he says.

 

L. Corbesier et al., “FT protein movement contributes to long-distance signaling in floral induction of Arabidopsis,” Science, 316:1030-33, 2007. (Cited in 144 papers)

 

References

1. J. Knott, “Effect of a localized photoperiod on spinach,” Proceedings of the Society for Horticultural Science, 31:152-54, 1934.

2. T. Huang et al., “The mRNA of the Arabidopsis gene FT moves from leaf to shoot apex and induces flowering,” Science, 309:1694-96, 2005.

3. S. Tamaki et al., “Hd3a protein is a mobile flowering signal in rice,” Science, 316:1033-36, 2007.

4. M. Lin et al., “FLOWERING LOCUS T protein may act as the long-distance florigenic signal in the cucurbits,” Plant Cell, 19:1488-506, 2007.

5. C. Li et al., “Wheat FT protein regulates VRN1 transcription through interactions with FDL2,” Plant Journal, 55:543-54, 2008.

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