Way back in time
It was the journey of one cell..
It was the journey of one cell..
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| picture courtesy: http://www.visualphotos.com |
and moved on to a journey of evolution..
Multicellularity was the destined goal
And
Humans were the last one in this series to evolve
and roam on the land..
Much have changed ever since..
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picture thankfully shared from:
http://www.bbc.co.uk/nature/
history_of_the_earth |
But..
We still have memories in each individual cell stored and intact,
like..
1. Our cells still do all life-activities in water..
2. Our multicellular journey in embryonic stage still starts with one cell,
bearing all features of their predecessor species at one or other stage..
(i.e. ontogeny repeats phylogeny)
bearing all features of their predecessor species at one or other stage..
(i.e. ontogeny repeats phylogeny)
3. And before coming to land, we still swim in sea-like water of amniotic fluid in mother's womb..
But..
Multicellularity has come up with unique features
for combined survival of trillions
of cell-fellows
for a common-cause,
like..
1. Multicellularity is the ultimate in cooperation,
multiple cells make up an individual
that cooperates for the benefit of the whole.
Sometimes cells give up their ability to reproduce for the benefit of
close kin..
2. Cells present in multicellular organisms possess the unique property of self-destruction.
They have the genetic information to commit suicide !
This phenomenon is termed as programmed cell death (PCD).
That way stressed and damaged cells kill them self for the benefit of whole..
They have the genetic information to commit suicide !
This phenomenon is termed as programmed cell death (PCD).
That way stressed and damaged cells kill them self for the benefit of whole..
And..
The whole lot of cells in an individual body are doom to die
And
Individuals have to perish !!
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The balance between the formation
of new cells and deletion of the
old
and abnormal cells is vital for all
physiological processes of the
body.
Credit: NIH
|
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The most mind-boggling
phenomenon in cells is the
mechanism through
which they
determine their own age, and
when old enough and susceptible
to damage, they commit suicide.
Every single day, millions of cells
die
and are replaced by new cells
―a process called cell turnover.
courtesy share:http://www.buzzle.com/
articles/why-do-cells-commit-suicide.html
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Intracellular regulators of the cell death program: All nucleated animal cells contain the seeds of their own destruction, in the form of various inactive procaspases that lie waiting for a signal to destroy the cell. It is therefore not surprising that caspase activity is tightly regulated inside the cell to ensure that the death program is held in check until needed.
Mitochondrial role in apoptosis: When cells are damaged or stressed, they can also kill themselves by triggering procaspase aggregation and activation from within the cell. In the best understood pathway, mitochondria are induced to release the electron carrier protein cytochrome c into the cytosol, where it binds and activates an adaptor protein called Apaf-1. This mitochondrial pathway of procaspase activation is recruited in most forms of apoptosis to initiate or to accelerate and amplify the caspase cascade. DNA damage, for example, can trigger apoptosis. This response usually requires p53, which can activate the transcription of genes that encode proteins that promote the release of cytochrome c from mitochondria. These proteins belong to the Bcl-2 family.
(http://www.ncbi.nlm.nih.gov/books/NBK26873/)
Cell suicide related disorder: One of the most disastrous consequences of failure in cell suicide is the dreadful set of diseases called cancer. Other conditions or disorders include congenital defects, like syndactyly (fused fingers), neural tube malformation, skeletal system defects, etc., as well as several autoimmune disorders. On the contrary, early triggering of cell suicide leads to degenerative disorders of the nervous and skeletal systems. (http://www.buzzle.com/articles/why-do-cells-commit-suicide.html)
Apoptosis and Cancer
Some viruses associated with cancers use tricks to prevent apoptosis of the cells they have transformed.
- Several human papilloma viruses (HPV) have been implicated in causing cervical cancer. One of them produces a protein (E6) that binds and inactivates the apoptosis promoter p53.
- Epstein-Barr Virus (EBV), the cause of mononucleosis and associated with some lymphomas
- produces a protein similar to Bcl-2
- produces another protein that causes the cell to increase its own production of Bcl-2. Both these actions make the cell more resistant to apoptosis (thus enabling a cancer cell to continue to proliferate).
- Some B-cell leukemias and lymphomas express high levels of Bcl-2, thus blocking apoptotic signals they may receive. The high levels result from a translocation of the BCL-2 gene into an enhancer region for antibody production.
- Melanoma (the most dangerous type of skin cancer) cells avoid apoptosis by inhibiting the expression of the gene encoding Apaf-1.
- Some cancer cells, especially lung and colon cancer cells, secrete elevated levels of a soluble "decoy" molecule that binds to FasL, plugging it up so it cannot bind Fas. Thus, cytotoxic T cells (CTL) cannot kill the cancer cells.
- Other cancer cells express high levels of FasL, and can kill any cytotoxic T cells (CTL) that try to kill them because CTL also express Fas (but are protected from their own FasL)
What makes a cell decide to commit suicide?
The balance between:
- the withdrawal of positive signals; that is, signals needed for continued survival, and
- the receipt of negative signals.
Withdrawal of positive signals
The continued survival of most cells requires that they receive
continuous stimulation from other cells and, for many, continued
adhesion to the surface on which they are growing.
Some examples of positive signals:
- growth factors for neurons
- Interleukin-2 (IL-2), an essential factor for the mitosis of lymphocytes
Receipt of negative signals
- increased levels of oxidants within the cell
- damage to DNA by these oxidants or other agents like
- accumulation of proteins that failed to fold properly into their proper tertiary structure
- molecules that bind to specific receptors on the cell surface and signal the cell to begin the apoptosis program.
These death activators include:
- Tumor necrosis factor-alpha (TNF-α) that binds to the TNF receptor;
- Lymphotoxin (also known as TNF-β) that also binds to the TNF receptor;
- Fas ligand (FasL), a molecule that binds to a cell-surface receptor named Fas (also called CD95).
Sydney Brenner, H. Robert Horvitz and John Sulston were awarded the
Nobel Prize in Physiology or Medicine in 2002 "for their discoveries
concerning genetic regulation of organ development and programmed cell
death."
― Nobelprize.org
― Nobelprize.org
some blog post links related with multicellularity, nature of mitochondria and viruses, cancer cause and cure.
