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Introduction to Apoptosis (Part Six)

By: Lionel Perez

Valenzuela Fetal Alcohol Syndrome

Ethyl alcohol (ethanol) is the main drug of abuse.

But not only affects young people and adults, infants also suffer from its effects, and approximately 1% of births in the U.S. have complications due to Fetal Alcohol Syndrome (FAS).

The SFA is a set of symptoms and signs affect children born to mothers who drank alcohol during pregnancy. They are generally low birth weight, small and often have birth defects and slow growth. The most serious problem is mental retardation.

grow When behavior problems are often severe, as evidenced by the statistics (94% of children with FAS have mental problems.)

FAS is the leading cause of preventable mental retardation.

For years the reasons why alcohol produced malformations were kept in the dark. However, after 2000, it was established that the damage result was that alcohol produced a distortion of the natural process of apoptosis. As we saw

apoptosis is crucial for normal development. It is a way to kill tumor cells and immune system cells that would otherwise attack the body itself is also so disposed of neurons that fail to make synapses with one another. When cells grow old, are eliminated by apoptosis in a natural way and can be replaced by new cells.

So what is the effect of alcohol on the nervous system of young embryos?

Kathleen Sulik, Martina Cartwright, Susan Smith and Marieta Heaton (all women!), Are the researchers who discovered over twenty years of research as alcohol induces the apoptosis of neurons (apoptotic neurodegeneration in the SFA).

Alcohol not only causes neurodegeneration and impaired nervous over in the system, but also extensive malformations of the face and skull (above the pictures of children with SFA).

More recently John Olney more accurately described the deleterious effects of alcohol. Alcohol, has powerful effects on the nervous system depressants, that's why they act in two ways, diminishes the power of the excitatory neurotransmitter glutamate and enhances the power depressant the neurotransmitter GABA.

words, all the actions of alcohol have in common decrease neuronal activity. This results in a fatal nervous system formation. Since neurons interpret this lack of activity-induced by alcohol, as a message of "kill" because they would not be forming synapses with other neurons, either in timing or in the correct sequence. Therefore apoptosis neurons are confused by this message in error caused by alcohol.

remember that the human brain neurons can have thousands of synaptic contacts and it is logical that the neurons that do not join this network, in the sequence and at the right time activate an apoptotic program.

Even small amounts of alcohol temporarily cause apoptosis of hundreds of thousands or millions of neurons. Because the brain of the developing fetus is particularly susceptible to this form of action.

Alcohol has these toxic effects at very early pregnancy (second week), long before a woman knows she is pregnant. Susceptibility to alcohol's toxic effects on neurons and other cells in formation, increases or decreases during pregnancy.

Considering that even with moderate drinking habits already kills neurons, it is advisable not to drink at all during pregnancy.

Our brain continues to mature and form new synapses, to three years or so (and continue forming new synapses until they die). So until three years after birth babies should not drink. Alcohol is not a game for a developing brain. Consider that adult drinkers looking for other people drink, including very young children who stay with consequences for the rest of their lives.

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Introduction to Apoptosis (Part Five)

By: Lionel Valenzuela Perez

activation of caspases

Apoptosis triggered by external signals: extrinsic or receptor pathway death

Fas and TNF receptors (receptor of tumor necrosis factor) are integral membrane proteins with receptor function domains exposed on the cell surface .

Binding of FasL death signaling molecules (Fas ligand) and TNF (tumor necrosis factor) to their respective receptors transmit a signal to the cytoplasm, which determines the activation of caspase 8 (an initiator caspase as caspase 9), which initiates a proteolytic cascade activating caspases that leads to phagocytosis of the cell.

When cytotoxic T cells, bind to target cells (eg virus infected cells or tumor cells to be destroyed), produce more FasL on their surface. By increasing the number FasL, increased binding to the Fas receptor on the target cell. The Fas receptor, activated by binding to FasL, triggers a signal that causes apoptosis.

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Introduction to Apoptosis (Part Four)

By: Lionel Perez Valenzuela

1) The apoptosis triggered by internal signals: the intrinsic pathway or mitochondrial pathway

Key Concepts in this way:

- The mitochondrion is a crucial point of control in the induction of apoptosis.

- Apoptosis is an active and controlled process that requires the synthesis of RNA and protein by the cell dying.

Components of the road:

a) The caspases: initiator and effector of apoptosis:

Caspases are proteases that have an amino acid cysteine \u200b\u200bin the active site, so are cysteine proteases. Any mutation affecting this amino acid to stop the protease inactive.

Caspases are named after more than a dozen of the same family proteases. The term refers to the spot where they cut (C) proteins after a amino acid aspartate (Asp), Caspases hence the name (other authors only refer to the term derives from caspase cysteine \u200b\u200baspartate proteases ).

These proteins can be divided into two groups initiator caspases (like caspase 9), which are activators of effector caspases (caspase 3).

The effector caspases are ultimately responsible to execute the cell, cleaving the protein that causes cell death. Because caspases can cause apoptosis, are closely regulated proteins. But then again, there needs to be activated if needed quickly. How is this done? In the first term does not regulate its transcription (caspases are present in virtually all cell types), but its activation to post-transcriptional level. Caspases are synthesized as pro-caspase immature. Ie need to be processed (cleaved) to become active.

b) Cytochrome c and Apaf-1, caspase 9 activators

Cytochrome c is a component of the respiratory chain, which acts as a proapoptotic factor when released into the cytoplasm. The release of cytochrome c, is preceded by changes in mitochondrial membrane permeability. Once released into citoplasama cytochrome c binds to the protein Apaf-1 (activating factor-1, apoptotic protease). This complex cytochrome c, Apaf-1 and oligomerize ATP and binds to the immature pro-caspase 9 activities, forms the apoptosome. The pro-active caspase-9 once it cleave to each other, forming the mature caspase (a tetramer with four subunits, two large and two small).

mature caspase 9 then initiates a proteolytic cascade that expands (amplification), activating other effector caspases (eg caspase 3), eventually leading to cellular changes characteristic of apoptosis.

c) Summary of the track

healthy cells, expressed on the surface of the outer mitochondrial membrane protein Bcl-2 . This protein in turn serves to anchor the protein Apaf-1 (activation factor-1 protease apoptotic). We can say that Bcl-2 protein is a protein inhibitor of apoptosis, because it holds to the Apaf-1 and prevents part of the apoptosome.

When generating internal damage cellular signals (eg free radical), the protein Bcl-2 protein released into the Apaf-1. A related protein called Bcl-2 Bax forms a pore and enters the mitochondrial membrane, causing the exit of cytochrome c (a component of the respiratory chain). Then, the protein is pro-apoptotic Bax, allowing exit of cytochrome c binding to Apaf-1.

released proteins, cytochrome c (plus the ATP required for activation) and Apaf-1 bind to the protease caspase 9. The result of the union of these three proteins cytochrome c, Apaf-1 and caspase 9, resulting in the formation of the complex called apoptosome.

The apoptosome begins proteolytic cascade that leads ultimately to the digestion of cytoplasmic structural proteins, structural proteins of the nucleus, degradation of the chromosomes and cell phagocytosis .

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Introduction to Apoptosis (Part Three)

By: Lionel Perez Valenzuela

Mechanism of apoptosis

Most cells need to survive a continuous stimulation of other cells, and many of them also need to be attached to the extracellular matrix.

Some of survival signals (positive signals) are:

a) growth factors and hormones.

b) Interleukin-2 (IL-2), which is essential for mitosis of lymphocytes.

Moreover cells also receive a steady stream of negative signals (signs of death), related in many cases aging cells or exposed to radiation or toxic chemicals, among them we can mention:

a) High levels of oxidants within the cell

b) Damage to DNA by oxidants or other agents such as ultraviolet light, x-rays, drugs, mutagenic

c) Accumulation of protein that fail to fold, so its tertiary structure is incorrect

Other death signals are mediated by certain molecules (ligands) that bind to specific receptors on the cell surface, to start the apoptotic program . That is, certain cell types undergo a selection according to their characteristics, some cells survive, whereas others were ordered activate the apoptotic program. These factors of death include:

- tumor necrosis factor alpha (TNF-alpha) that binds to TNF.

- The lymphotoxin (also known as TNF-beta) that also binds to TNF receptor.

- Fas ligand (Fas L), a molecule that binds to surface receptor known as Fas (also known as CD95).

For example in the immune system to eliminate autoreactive cells (ie that can attack the body itself) through apoptosis, and allows cells to survive that distinguish self from foreign. They were also directed to transformed cells (tumor), activate the apoptotic program. During maturation of the nervous system, a large number of neurons undergoing apoptosis, not receiving appropriate survival stimuli, did not form correct synapses.

Therefore the survival of the cell is determined by a balance between the positive signs of survival (presence or absence) and the receipt of negative signals.

Molecular mechanisms of apoptosis

There are basically two major molecular mechanisms by which a cell commits apoptosis.

1) Via intrinsic or mitochondrial pathway : death signals that occur within the cell.

2) extrinsic or death receptor : death-activating signals arriving from abroad. These signals binds to receptors on the cell surface.

In the next article we will see in detail, how they act at the molecular level the intrinsic (mitochondrial) and extrinsic (receptor demuerte).

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Introduction to Apoptosis (Part One)

By: Lionel Perez Valenzuela

Why cells die?

Cells die in two basic forms, die due to damage and injuries they have suffered, a process called necrosis or induced to commit "suicide" slow and regulated process known as apotosis or programmed cell death.

In Greek classic apoptosis means "fall" in analogy with the falling leaves of autumn trees or petals in flowers. This analogy reinforces the idea that cell death is an integral and necessary part of the life cycle of living beings.

Injury Death

The damage that can receive a cell can be of different types, damage mechanical, ischemia (lack of oxygen) or can be exposed toxic elements.

The cell necrosis is a passive victim. Cells that receive these attacks, suffering a series of updates feature. To break the membrane of cells and their organelles (like mitochondria) swell, as they have lost the ability to regulate the passage of ions and water. Finally, the cell ruptures, releasing its contents that may cause inflammation in surrounding tissues.

Upon inflammatory signals, macrophages and other white blood cells converge in necrotic cells and ingested. Inflammation contributes to limit the infection and remove debris, but the action and the secretions of the white blood cells can damage normal tissue.

Death by "suicide"

Apoptosis is an active process that requires Cell waste energy in their own demise. It is accompanied by specific morphological changes, cell loss volume ( shrinks), it departs from neighboring cells and appear to boil as on its surface are "bubbles."

The cell nucleus, undergoes major changes, initially chromatin condenses and drops out of the nuclear envelope. Mitochondria break down and release the c itocromo c. The plasma membrane may also undergo changes, as exposure to the outer surface of the phospholipid phosphatidylserine , normally found on the inside of the membrane (plasma membrane asymmetry).

These cells are dying and giving their Phosphatidylserines can be recognized by neighboring cells or scavenger cells that have receptors for phosphatidylserine. These phagocytic cells such as macrophages and dendritic Ceulaer, which are present in all tissues, phagocytose apoptotic cells without causing inflammatory response, and that release cytokines that inhibit inflammation (IL-10 and TGF-beta).

Other non-apoptotic cells ingested continue undergoing new changes. Chromatin and fragmented nucleus with the rest of the cell is divided into numerous apoptotic bodies, which may contain one or two fragments nuleares. These bodies in turn may be ingested by phagocytic cells without causing inflammation.

Finally we know that certain cells undergoing programmed death are not phagocytosed but may persist indefinitely. One such case is the lens of the eye, whose cells replaced most of its cytoplasm by the protein crystal, when they die, Another case of skin cells, called keratinocytes, which are generated from precursors of a deeper layer and then migrate to the surface, dying on the road. These cells cytoplasmic keratin content. These dead cells form the outer protective layer of the skin to fall off and are replaced by other keratinocytes.

events leading to programmed cell death follow a pattern ordered as specific and can be compared with those of cell mitosis.

I leave here a few videos (later will add others, as progress with the subject.) Are English and German. As I can I will put the subtitles in Castilian.

This video is just to link it, and this in German. A little patience, for the clarity of the filming of the cell into apoptosis is worth it.

http://www.youtube.com/watch?v=E5e1jbFYjD4&feature=related

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Mother of Thousands, Mother of millions!

By: Lionel Perez Valenzuela

That rarest plant!

certainly Kalanchoe daigremontiana, give that impression when one looks at it. With all those little "seedlings" growing on the edge of the leaves. It looks very strange. Each time one of these small seedlings (propagules) from the edge of the leaves off, is likely to be achieved a mature plant. This form of reproduction property of Kalanchoe daigremontiana is asexual and highly efficient.

An exotic and toxic plant!

The Kalanchoe is native to Madagascar, is extremely durable and has spread to many regions of the world. Reproduces very quickly (as it says its common name "mother of thousands") and is toxic because it contains a cardiac glycoside, the Daigremontianina . is common in some regions of the world who suffer livestock property poisoning by eating this plant.

How do plants reproduce?

A very basic level we can say that plants can reproduce sexually or asexually. In sexual reproduction, they are very different haploid cells called gametes. fusion of male and female gametes leads to the development of an embryo (zygotic embryo) and then to the formation of the seed. But in
asexual reproduction, new plants arise through specialized vegetative organs, consisting of somatic cells, such as tubers, rhizomes, stolons, bulbs, etc. Although also can do so by other methods such as natural somatic embryogenesis (somatic embryo).

Therefore plants can develop two types of embryos, zygotic embryos (from sexual reproduction) and somatic embryos (by asexual reproduction). The plants that developed from zygotic embryos possess characteristics of both parents, however those that are formed from somatic embryos are genetically identical your parent (clones). Recall that in plants embryos are bipolar. A pole has the apical meristem that give rise to leaves and stems and the other pole has the root meristem that give rise wing roots.

In certain plants is very common the formation of somatic embryos, including seeds. For example, citrus fruits, where both types of embryos are formed almost simultaneously.

How they grow and develop plants?

Plants and animals grow and develop, but they do it differently. Formation in plants of organs (organogenesis) is performed post-embryonic development (embryogenesis). So we could say that plants have two programs, one organogenic and embryogenic another.

embryogenesis and organogenesis are separate processes in plants.

When a plant reproduces in a sexual way, occurs egg fertilization (through pollination), we obtain the zygote, an embryo develops, the seed (the process of seed formation it is called, embryogenesis), the accessory structures and the fruit.

embryos in plants must go through a process of desiccation (water loss) essential for cellular metabolism stop and the seed is in a dormant state until it is reactivated. Therefore seed with its embryo is capable of withstanding until the fruit ripens, falls, breaks down, the seed is free and eventually (if they found an appropriate way) when in contact with water reactive metabolism begins to germinate and grow the seedling from the embryo (this process will be called organogenesis).

Consider for a moment how important it is that the seed pass through a dormancy period of apparent inactivity, because it can store and transport the seeds for planting in the right time.

What are meristems?

All plants have the same basic pattern of body schema, consisting of repeating units of stem and leaf. As we said before these units of stem and leaf, stem from the apical meristem, while roots grow from the root tips.

The outbreak apical meristem or bud (in English, shoot apical meristem or SAM, in its abbreviation), contains in its center, a group of stem cells, totipotent undifferentiated, which is self-renewing. As stem cells divide, daughter cells are pushed to the edge of the meristem, where clusters of these cells, they differ in leaf founder cells.

We can therefore say that the meristem tissues are formed by a group of totipotent cells, undifferentiated , which is self-renewing and generating other cell types that in turn will form the various tissues and organs plants.

Both apical meristem as the root, are generated during embryogenesis (formation of the seed), but do not participate in embryo development. The meristems are activated once the seedlings have germinated and remained active throughout the life of the plant, being a reservoir of new cells for organogenesis (development of stem, leaves, flowers).

totipotency in plant cells.

somatic cells of plants , unlike cells somatic animals have a remarkable feature , can regenerate a complete organism. This potential for regeneration is called totipotency.

This ability of plants is widely used to multiply asexually, for example from somatic embryos. So from a single plant in a laboratory, can be grown hundreds of plants genetically identical to the parent plant and repeat this process again and again.

Control of embryogenesis and organogenesis in plants.

varis genes have been identified master regulators of organogenesis and plant embryogenesis. One of the most important is the gene STM (Shoot Meristemless), a gene similar to the homeotic genes Knotted1 (English Knotted1-like homeobox). These genes generally are called genes KNOX1. We will see in another series of articles that homeotic genes control development in plants and animals. In this case when the STM gene is mutated, the apical meristem (SAM remember that shorten), not formed and therefore the plants can not grow and remain in the seed stage. Then we can say that the STM gene is important for organogenesis. Furthermore, when this gene is establishing he sobreeexpresa plants show growth buds ectopic (misplaced) in the leaves.

Genes essential for the formation of both types of embryos (somatic and zygotic) are the LEC1 (Leafy Cotyledon 1) and Fus3. If these genes are mutated the embryos stop their development, are intolerant to desiccation and therefore unworkable. When these genes are overexpressed in transgenic plants ectopically form somatic embryos from vegetative cells.

Interestingly, ectopic overexpression of either the genes that control organogenesis (STM) and embryogenesis (LEC1, Fus3), forcing the vegetative cells of genetically modified plants to form structures similar to the seedlings of Kalanchoe daigremontiana. So the researchers decided to study the activity of STM genes, LEC1 and Fus3 directly on the seedlings, so check directly which are the genetic programs involved in its formation.

plants of the genus Kalanchoe, an excellent experimental model.

the genus Kalanchoe plants show different strategies evolutive

1 - Species that reproduce only sexually and are not seedlings. Therefore zygotic embryos can form and have the LEC1 gene active.

2 - Species like the Kalanchoe daigremontiana only reproduce asexually and form seedlings at the edge of the leaves, constitutively. All these species have the LEC1 gene mutated, and possibly inactive or altered function. These plants can not form embryos (hence the seeds are viable).

3 - Species that can reproduce sexually (form viable seeds) and semiconstitutiva produce seedlings as well as in situations of stress. LEC1 gene active. These species like the Kalanchoe gastonis-bonnieri, which has all the reproductive strategies represent the ancestral evolutionary line.

4 - species that reproduce sexually, but that under conditions of stress can produce seedlings. LEC1 gene active.

Evolution asexual reproduction in Kalanchoe.

As we saw daigremontana Kalanchoe, is reproduced only asexually , seeds and embryos is not normal, but on the contrary, these seedlings develop very small (their chips seem cotyledons), which still attached to the mother plant, begin to form adventitious roots. At no time suffer desiccation, but they have their own transport system and even seem, are not embryos.

Why does this process of reproduction asexual? Well apparently some plants of this genus, have lost the ability to reproduce sexually, as they have the mutated gene LEC1 key in the formation of seeds and therefore have adapted to asexual reproduction. Or, conversely, may be that the mutation somehow LEC1 favors asexual reproduction.

most recent studies have shown that Kalanchoe daigremontiana plantlets form at the edge of the leaves, because both programs the organogenic and embryogenic work cooperatively on the sheet. These conclusions are based on three points:

1 - Kalanchoe daigremontiana STM gene can initiate a process of developmental change and generate a group of undifferentiated cells and competent as a meristem at the edge of the leaves (organogenic program).

2 - STM gene deletion prevents the development of the seedlings at the edge of the leaves.

3 - Both the LEC1 gene (mutated) as the Fus3 gene is expressed actively in the formation of the seedlings (embryogenic program), and therefore have been recruited into the organogenic program of development of seedlings, and would be responsible for some of the These unique features of somatic propagules (embryo-like structure).

The evidence provided suggests that asexual reproduction then it probably began as a process of organogenesis then recruited an embryogenesis program into the leaves, in response to the loss of the ability of sexual reproduction this genre.

important Why are these jobs?

The answer is simple, help us to understand how plants reproduce, evolve and adapt. Little-known phenomena and poorly understood at present.

addition there is enormous interest in the production of plants from somatic embryos, artificial seed technology, plant breeding endangered or displaced native. Propagation of fish with high commercial value, hybrid selection, reproduction studies of genetically engineered plants, sanitation, disease, etc, etc, etc. All these technologies could have a major impact on our ability to produce seeds and plants more resistant on the market value or food and therefore affect our ability to provide more and better food of plant origin is a growing population with an environment increasingly degraded.

Source: MP Helena Garces, Neelima R. Sinha (2007) Proc Natl Acad Sci USA, vol 104:15578-15583