Scientists Discover Possible Reason for Neurodegenerative Disorders

First Posted: Apr 11, 2016 07:10 AM EDT
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Cells were usually meant to live, but some were meant to die. Caenorhabditis elegans was a tiny worm that was a favored subject organism for biologists. Its linker cells was among those programmed for cell termination.

The cell helped determine the form of gonads in male worms. The cell will then die after two days as the worms will shift from larvae into adults. This cell's predestined death was a normal stage in the animal's development, but the molecular and genetic mechanisms behind it have yet to be worked out.

Shai Shaham, head of the Scientists in Rockefeller University's Laboratory of Developmental Genetics, had previously discovered that the linker cell did not expire through apoptosis, which was a more common form of predetermined cell death. Every detail about the death process was different from apoptosis. It looked different under the microscope and it required different genes and kinetics, according to a feature from Science Daily.

Cell death had been observed and described in the artificial setting of a tissue culture dish, but not within a living body. The Shaham lab had been able to analyze the molecular mechanism that caused linker cell death in worms. Their results suggested that the newly discovered cell dying process resembled that which led to the loss of neurons and neuronal parts in people with various neurodegenerative disorders.

To determine the molecular processes that resulted in linker cell death, the team introduced random mutations in worms and then looked for animals in which the linker cells survived for a longer time period. They identified various mutations that prolonged the survival of cells, including one that affected the mechanisms of HSF-1, a protein discovered to shield cells from stresses like heat.

The cells study found that HSF-1, which typically performed a protective role in the cell, was discovered to be a key regulator of the cell death, according to a feature from Newswire.

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