How our cells get rid of junk and recycle

University of Michigan researchers have figured out a way to manipulate lysosomes. This could change the way common diseases such as neurodegenerative diseases are treated.
Written by Boonsri Dickinson, Contributing Editor

Ever wonder what happens to the rubbish inside your body? The small pouch hidden inside your cells is called the lysosome and it acts as the garbage disposal and the recycling center.

From the recycled bits, the cell rebuilds the body.

When cells mess up, genetic mutations and out of whack proteins are created. Fortunately, cells, by nature, are rather self-destructive.

As we age, our cells lose the ability to cannibalize and aren't as good at disposing of the cellular garbage.

Dysfunctional lysosomes have been linked to over 50 disorders. Doctors can treat them by giving people the proteins they are deficient in. And knowing more about lysosomes might help in cancer prevention and aid in delaying the onset of Alzheimer's disease.

The thing is, we don't know that much about lysosomes. Scientists know what happens with calcium channels in muscle and nerve cells, but it's anyone's guess how the calcium channels function inside a lysosome.

In the labs at the University of Michigan, researchers uncovered some of the mystery surrounding lysosomes. To do so, cell biologist Haoxing Xu looked at the calcium channels in them.

By using a pipette, the researchers hooked up electrodes to a cell membrane to record the protein activity.

Xu found that a protein called TRPML1 acts as a calcium channel in lysosomes. The lipid called PI(3,5)P2, sends a signal that activates the protein.

Mutations in the gene that produces the protein and mutations in the enzymes that produce the lipid have been linked to diseases that cause mental retardation and neurodegeneration.

Therefore, tweaking TRPML1 through the use of channel activators or inhibitors could manipulate membrane traffic and prevent the development of diseases.

"If you can activate the channel, it might be possible to overcome the membrane traffic defects caused by the disease-causing mutations. Luckily, small-molecule chemicals that can stimulate TRPML1 channel activity are already available, " Xu said in a statement.

IThe Michigan researchers are currently trying to see if manipulating the TRPML1 channel can stop or reverse the development of Amyotrophic lateral sclerosis (ALS) in mice models.

"If the system we're studying turns out to be compromised in more common diseases, the method of increasing channel activity could have important implications for their treatment," he said.

Credit: Xiang Wang and Haoxing X

This post was originally published on Smartplanet.com

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