Tuesday 2 August 2011

Regulation of carotenoid synthesis and accumulation in plants

The amounts and identities of the various carotenoids in the photosynthetic membranes of green plants
are relatively well conserved. A handful, typically including lutein, β-carotene, violaxanthin, neoxanthin,
and zeaxanthin, account for most of the carotenoid pigment in the chloroplasts of many plant and
algal species [1]. The biosynthesis and accumulation of these carotenoids in developing chloroplasts
proceed in concert with the assembly of the light-harvesting antennae and reaction centers with which
these pigments are in large part associated [2]. Genetic modifications that reduce or prevent synthesis
of one or more of these carotenoids may be compensated by increases in others so that the total
carotenoid content in the photosynthetic membranes is not much affected [3–7]. Such observations
make clear that robust feedback mechanisms exert control over carotenoid synthesis and accumulation
in plant chloroplasts.
Carotenoid pigmentation in non-green plant plastids, in contrast, ranges broadly both in quantity
and composition. The total amount of the carotenoids may vary from little or none (as in white flower
petals) to quite substantial quantities (as in the dark orange petals of certain marigold varieties). The
pigments may include those common in the photosynthetic membranes (e.g., the lutein of marigold
flower petals), consist of earlier pathway intermediates (e.g., lycopene in red tomato fruits), or be
derived from carotenoids normally found in the chloroplasts (e.g., capsanthin and capsorubin, formed
from violaxanthin in red pepper fruits).
What mechanisms are employed by plants to specify and adjust the amounts and identities of the
various carotenoids that are accumulated in green and non-green plastids? The answer to this question
has many parts, and much remains to be learned. There is abundant evidence to indicate that the reaction
catalyzed by phytoene synthase (PSY) is an important control point for regulation of flux into and
through the carotenoid pathway [8]. This reaction will not be discussed here. Instead, following a brief
update on genes and enzymes of the pathway, I will review what has been learned recently regarding
two other likely control points of the carotenoid pathway in plants: the availability of substrate and
branching of the pathway.

Table 1 Carotenoid pathway genes in Arabidopsis thaliana.
Gene Enzyme Family Members*
Ipi isopentenyl diphosphate isomerase 2
Ggps geranylgeranyl diphosphate synthase 11
Psy phytoene synthase 1
Pds phytoene desaturase 1
Zds ζ-carotene desaturase 1
CrtISO carotene isomerase 1
Ptox plastid terminal oxidase 1
Lcy-b lycopene β-cyclase 1
Lcy-e lycopene ε-cyclase 1
Chy-b β-ring hydroxylase 2
Chy-e ε-ring hydroxylase not identified
Zep zeaxanthin epoxidase 1
Vde violaxanthin de-epoxidase 1
Nsy neoxanthin synthase no ortholog

Carotenoids are isoprenoids. The five carbon building blocks that serve as precursors for the synthesis
of carotenoids and other isoprenoid compounds, isopentenyl diphosphate (IPP) and dimethylallyl
diphosphate (DMAPP), are produced in two different compartments and by two different pathways in
plant cells (Fig. 1). The well-known mevalonate (MVA) pathway in the cytosol/endoplasmic reticulum
begins with acetyl-CoA and proceeds in linear fashion to IPP, which is then reversibly converted to
DMAPP in a reaction catalyzed by IPP isomerase (IPI) [15].
The recently recognized methylerythritol (MEP) pathway occurs in plant plastids, in cyanobacteria,
and in certain other bacteria [16; see 17 for a recent update on this incompletely elucidated pathway],
and utilizes pyruvate and glyceraldehyde-3-phosphate (GAP) as the initial substrates (Fig. 1). In
contrast to the MVA pathway, DMAPP and IPP are produced separately via a branching of the MEP
pathway [18]. Even so, IPP isomerase, the enzyme that serves as the terminal enzyme of the cytosolic
MVA pathway (Fig. 1), is also present in plastids [19,20].
Carotenoids in plants are synthesized in the plastids. Are the IPP and DMAPP utilized for
carotenoid synthesis produced solely via the plastid MEP pathway or does the cytosolic MVA pathway
also contribute? Does the source of IPP/DMAPP for plastid isoprenoid synthesis depend on the stage
of development, the type of tissue, or the type of plastid (e.g., etioplast, chloroplast, chromoplast, or
Although there are some indications of compartmental “crosstalk”, isoprenoid synthesis in both
green and non-green plastids of many plants has been found to rely primarily on IPP and DMAPP produced
via the MEP pathway. Much of the evidence in support of an MEP pathway origin for plastid isoprenoids
comes from analyses of the distribution of label in certain isoprenoid pathway end-products
after incubation of plants or algae with 13C-labeled glucose or 13C-labeled 1-deoxy-D-xylulose (DOX)
[reviewed in 21]. The effects of specific MVA and MEP pathway inhibitors and the phenotypic consequences
of a mutation in an Arabidopsis gene encoding the MEP pathway enzyme deoxyxylulose-5-
phosphate synthase (DXS) lend further support. The application of the MEP pathway inhibitor fosmidomycin
(an inhibitor of deoxylulose-5-phosphate reductoisomerase, DXR, the first enzyme specific
to the MEP pathway; see Fig. 1) reduces lycopene accumulation in tomato fruits [22], whereas the MVA
© 2002 IUPAC, Pure and Applied Chemistry 74, 1409–1417
Regulation of carotenoid synthesis and accumulation in plants 1411
Fig. 1 Distinct isoprenoid pathways exist in plastids and cytosol of plant cells. Enzymes that may limit flux through
the MEP pathway (the evidence is largely from studies of the bacterium E. coli) are in white text in black boxes.
Abbreviations: diPG, diphosphoglyceraldehyde; GAP, glyceraldehyde-3-phosphate; GAPD, glyceraldehyde-3-
phosphate dehydrogenase; HMG, hydroxymethylglutaryl; MEP, methylerythritol-5-phosphate; PEP, phosphoenolpyruvate.

Troponin I and troponin T

If you had a heart attack, you will need to stay in the hospital, possibly in the intensive care unit (ICU). You will be hooked up to an ECG machine, so the health care team can look at how your heart is beating.
Life-threatening irregular heartbeats (arrhythmias) are the leading cause of death in the first few hours of a heart attack. These arrythmias may be treated with medications or electrical cardioverson/defibrillation.
The health care team will give you oxygen, even if your blood oxygen levels are normal. This is done so that your body tissues have easy access to oxygen and your heart doesn't have to work as hard.
An intravenous line (IV) will be placed into one of your veins. Medicines and fluids pass through this IV. You may need a tube inserted into your bladder (urinary catheter) so that doctors can see how much fluid your body removes.
Angioplasty, also called percutaneous coronary intervention (PCI), is the preferred emergency procedure for opening the arteries for some types of heart attacks. It should preferably be performed within 90 minutes of arriving at the hospital and no later than 12 hours after a heart attack.
Angioplasty is a procedure to open narrowed or blocked blood vessels that supply blood to the heart.
A coronary artery stent is a small, metal mesh tube that opens up (expands) inside a coronary artery. A stent is often placed after angioplasty. It helps prevent the artery from closing up again. A drug eluting stent has medicine in it that helps prevent the artery from closing.
Depending on the results of the ECG, certain patients may be given drugs to break up the clot. It is best if these drugs are given within 3 hours of when the patient first felt the chest pain. This is called thrombolytic therapy. The medicine is first given through an IV. Blood thinners taken by mouth may be prescribed later to prevent clots from forming.
Thrombolytic therapy is not appropriate for people who have:
  • Bleeding inside their head (intracranial hemorrhage)
  • Brain abnormalities such as tumors or blood vessel malformations
  • Stroke within the past 3 months (or possibly longer)
  • Head injury within the past 3 months
Thrombolytic therapy is extremely dangerous in women who are pregnant or in people who have:
  • A history of using blood thinners such as coumadin
  • Had major surgery or a major injury within the past 3 weeks
  • Had internal bleeding within the past 2-4 weeks
  • Peptic ulcer disease
  • Severe high blood pressure
Many different medicines are used to treat and prevent heart attacks. Nitroglycerin helps reduce chest pain. You may also receive strong medicines to relieve pain.
Antiplatelet medicines help prevent clots from forming. Aspirin is an antiplatelet drug. Another one is clopidogrel (Plavix). Ask your doctor which of these drugs you should be taking. Always talk to your health care provider before stopping either of these drugs.
  • For the first year after a heart attack, you will likely take both aspirin and clopidogrel every day. After that, your health care provider may only prescribe aspirin.
  • If you had angioplasty and a coronary stent placed after your heart attack, you may need to take clopidogrel with your aspirin for longer than one year.
Other medications you may receive during or after a heart attack include:
  • Beta-blockers (such as metoprolol, atenolol, and propranolol) help reduce the strain on the heart and lower blood pressure.
  • ACE inhibitors (such as ramipril, lisinopril, enalapril, or captopril) are used to prevent heart failure and lower blood pressure.
  • Lipid-lowering medications, especially statins (such as lovastatin, pravastatin, simvastatin, atorvastatin, and rosuvastatin) reduce blood cholesterol levels to prevent plaque from increasing. They may reduce the risk of another heart attack or death.
Always talk to your health care provider before stopping any medications, especially these drugs. Stopping or changing the amount of these medicines can be life threatening.
Coronary angiography may reveal severe coronary artery disease in many vessels, or a narrowing of the left main coronary artery (the vessel supplying most of the blood to the heart). In these circumstances, the cardiologist may recommend emergency coronary artery bypass surgery (CABG). This procedure is also called "open heart surgery." The surgeon takes either a vein or artery from another location in your body and uses it to bypass the blocked coronary artery.

Support Groups

See:Heart disease -- resources

Outlook (Prognosis)

How well you do after a heart attack depends on the amount and location of damaged tissue. Your outcome is worse if the heart attack caused damage to the signaling system that tells the heart to contract.
About a third of heart attacks are deadly. If you live 2 hours after an attack, you are likely to survive, but you may have complications. Those who do not have complications may fully recover.
Usually a person who has had a heart attack can slowly go back to normal activities, including sexual activity.

Possible Complications

  • Cardiogenic shock
  • Congestive heart failure
  • Damage extending past heart tissue (infarct extension), possibly leading to rupture of the heart
  • Damage to heart valves or the wall between the two sides of the heart
  • Inflammation around the lining of the heart (pericarditis)
  • Irregular heartbeats, including ventricular tachycardia and ventricular fibrillation
  • Blood clot in the lungs (pulmonary embolism)
  • Blood clot to the brain (stroke)
  • Side effects of drug treatment

When to Contact a Medical Professional

Immediately call your local emergency number (such as 911) if you have symptoms of a heart attack.


To prevent a heart attack:
  • Keep your blood pressure, blood sugar, and cholesterol under control.
  • Don't smoke.
  • Consider drinking 1 to 2 glasses of alcohol or wine each day. Moderate amounts of alcohol may reduce your risk of cardiovascular problems. However, drinking larger amounts does more harm than good.
  • Eat a low-fat diet rich in fruits and vegetables and low in animal fat.
  • Eat fish twice a week. Baked or grilled fish is better than fried fish. Frying can destroy some of the health benefits.
  • Exercise daily or several times a week. Walking is a good form of exercise. Talk to your doctor before starting an exercise routine.
  • Lose weight if you are overweight.
If you have one or more risk factors for heart disease, talk to your doctor about possibly taking aspirin to help prevent a heart attack. Aspirin therapy (75 mg to 325 mg a day) or another drug such as prasugrel or clopidogrel may be prescribed.
New guidelines no longer recommend hormone replacement therapy, vitamins E or C, antioxidants, or folic acid to prevent heart disease.
After a heart attack, you will need regular follow-up care to reduce the risk of having a second heart attack. Often, a cardiac rehabilitation program is recommended to help you gradually return to a normal lifestyle. Always follow the exercise, diet, and medication plan prescribed by your doctor.

Alternative Names

Myocardial infarction; MI; Acute MI; ST-elevation myocardial infarction; non-ST-elevation myocardial infarction
 et al. Acute ST-segment elevation myocardial infarction: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th edition). Chest. 2008;133:708S-775S.