FROM NERVE ROOTS TO PLANT ROOTS - RESEARCHERS ARE GAINING UNEXPECTED INSIGHTS INTO HEREDITARY SPASTIC PARAPLEGIA

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FROM NERVE ROOTS TO PLANT ROOTS - RESEARCHERS ARE GAINING UNEXPECTED

INSIGHTS INTO HEREDITARY SPASTIC PARAPLEGIA

NIHPRESS

Thursday, August 6, 2009, 9:13 AM

 

U.S. Department of Health and Human Services

NATIONAL INSTITUTES OF HEALTH NIH News

National Institute of Neurological Disorders and Stroke (NINDS)

<http://www.ninds.nih.gov/>

Embargoed for Release: Thursday, August 6, 2009, Noon, EDT

 

CONTACT: Daniel Stimson, NINDS, 301-496-5751 <e-mail: stimsond

 

FROM NERVE ROOTS TO PLANT ROOTS - RESEARCHERS ARE GAINING UNEXPECTED INSIGHTS

INTO HEREDITARY SPASTIC PARAPLEGIA

 

Sprouting. Branching. Pruning. Neuroscientists have borrowed heavily from

botanists to describe the way that neurons grow, but analogies between the

growth of neurons and plants may be more than superficial. A new study from the

National Institutes of Health and Harvard Medical School suggests that neurons

and plant root cells may grow using a similar mechanism.

 

The research also sheds light on the hereditary spastic paraplegias (HSP), a

group of inherited neurological disorders in which some of the longest neurons

in the body fail to grow and function properly. The genes behind HSP and their

roles inside neurons are poorly understood. However, the study suggests that

several forms of HSP share an underlying defect with each other - and with

abnormal root hair development in a plant widely used for agricultural research.

 

The strange implication is that the plant, Arabidopsis thaliana (mouse-ear

cress), could prove useful for further research on HSP.

 

" This study provides us with valuable new insights that will stimulate research

toward therapies for hereditary spastic paraplegias, " says Craig Blackstone,

M.D., Ph.D., an investigator at NIH's National Institute of Neurological

Disorders and Stroke (NINDS) and an HSP expert. Dr. Blackstone performed the

study in collaboration with William Prinz, Ph.D., an investigator at the NIH's

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), and

Tom Rapoport, Ph.D., a Howard Hughes Medical Institute investigator and a

professor of cell biology at Harvard Medical School.

 

HSP primarily affects corticospinal neurons, which extend projections called

axons from the brain's cerebral cortex to the spinal cord. The longest

corticospinal axons extend nearly all the way down the spinal cord - a distance

up to about three feet - in order to control movement in the legs. In HSP, these

long axons develop abnormally or they degenerate later in life, causing muscle

stiffness and weakness in the legs. HSP exists in many forms in different

families, and more than 40 genes have been implicated in the disease.

 

In the new study, published in Cell, the researchers propose that defects in the

shaping of a subcellular structure known as the endoplasmic reticulum (ER) are a

common cause of HSP. The ER - named for its reticulated (or net-like) shape - is

a cellular factory, where molecules such as proteins and lipids that are vital

to cell growth are made and packaged for shipping to various cellular

destinations. The researchers theorize that in several forms of HSP, the ER

loses its complex shape and is unable to support the growth or maintenance of

long corticospinal axons.

 

 

 

Several years ago, other researchers showed that similar ER defects in

Arabidopsis impair the growth of the plant's root hairs. These are wispy,

microscopic projections that grow from the plant's individual root cells.

 

The new study focuses on a gene called atlastin. This gene is defective in about

10 percent of HSP cases, and in previous research, Dr. Blackstone's group showed

that it has a role in axon growth. The new study reveals that the atlastin

protein is necessary for maintaining the shape of the ER in mammalian cells, and

that an analogous protein called Sey1p performs the same function in baker's

yeast. 

 

The researchers demonstrate that ER shaping defects have general relevance for

HSP, by showing a connection between atlastin and a group of proteins known as

the DP1 family. Years ago, Drs. Prinz and Rapoport reported that a yeast analog

of DP1 regulates the shape of the ER in yeast. Meanwhile, others researchers had

independently reported that mutations in REEP1, a member of the DP1 family,

cause 3 percent to 8 percent of HSP cases. The new study shows that atlastin

interacts physically with DP1 in mammalian cells, and that Sey1p (the yeast

atlastin) interacts with the DP1 analog in yeast.

 

Finally, Dr. Blackstone's study notes that Arabidopsis has an analog of

atlastin, called Root Hair Defective 3 (RHD3). Mutations affecting RHD3 cause

the plant to grow short, wavy root hairs.

 

If this connection between axon growth and root hair growth withstands further

study, Arabidopsis could be a useful tool for investigating mechanisms of HSP.

Arabidopsis is easy to raise in the lab, and the short root hairs of the RHD3

mutant are easy to observe, compared to the growth defects in atlastin-deficient

neurons and yeast. Dr. Blackstone hopes to collaborate with other researchers to

initiate a search for genes and compounds that correct root hair development in

the RHD3 mutant, which might provide valuable therapeutic insights into HSP.

 

(HTML version includes photo):

<http://www.ninds.nih.gov/img/neurons_roots_HSP.jpeg>

The photo caption is:  Top: Rat cortical neurons. Bottom: Arabidopsis roots.

Left side shows normal neurons and root hairs. Right side shows the effects of

atlastin/RHD3 deficiency, with shortening of both and waviness of root hairs.

Neuron images courtesy of Dr. Craig Blackstone, NINDS. Arabidopsis images

courtesy of Dr. John Schiefelbein, University of Michigan, Ann Arbor.

 

Reference:  Hu J, Shibata Y, Zhu P-P, Voss C, Rismanchi N, Prinz W, Rapoport TA,

and Blackstone C.  " A Class of Dynamin-Like GTPases Involved in the Generation

of the Tubular ER Network. "   Cell, Vol. 138, August 7, 2009.

 

NINDS <www.ninds.nih.gov> is the nation's primary supporter of biomedical

research on the brain and nervous system. NIDDK <www.niddk.nih.gov> conducts and

supports basic and clinical research and research training on some of the most

common, severe and disabling conditions affecting Americans. The Institute's

research interests include: diabetes and other endocrine and metabolic diseases;

digestive diseases, nutrition, and obesity; and kidney, urologic and hematologic

diseases.

 

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency

-- includes 27 Institutes and Centers and is a component of the U.S. Department

of Health and Human Services. It is the primary federal agency for conducting

and supporting basic, clinical and translational medical research, and it

investigates the causes, treatments, and cures for both common and rare

diseases. For more information about NIH and its programs, visit <www.nih.gov>.

 

##

 

This NIH News Release is available online at:

<http://www.nih.gov/news/health/aug2009/ninds-06.htm>.

 

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