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JCI online early table of contents: Oct. 12, 2009

EDITOR'S PICK: A balancing act in Parkinson disease: phosphorylation of alpha-synuclein

Both genetic and pathologic data indicate a role for the neuronal protein alpha-synuclein in Parkinson disease. Previous studies have indicated that phosphorylation of alpha-synuclein at amino acid 129 (Ser129) is a key event in alpha-synucleinmediated nerve cell toxicity. However, Mel Feany and colleagues, at Brigham and Women's Hospital, Boston, have now identified a counterbalancing role in nerve cell protection for phosphorylation of alpha-synuclein amino acid 125 (Tyr125).

In the study, phosphorylation of human alpha-synuclein Tyr125 was detected in Drosophila transgenic for human alpha-synuclein and shown to protect from alpha-synucleinmediated nerve cell toxicity in a Drosophila model of Parkinson disease. That the two phosphorylated amino acids have opposing roles was indicated by the observation that Tyr125 phosphorylation decreased levels of toxic soluble alpha-synuclein oligomers in the Drosophila brain, whereas Ser129 phosphorylation increased them. More importantly, Tyr125 phosphorylation was found to decrease as both humans and Drosophila aged and was reduced in cortical tissue from patients with synucleinopathy dementia with Lewy bodies, a disease related to Parkinson disease. The authors therefore suggest that changes in the balance between Ser129 and Tyr125 phosphorylation which promote nerve cell toxicity and protection, respectively might cause alpha-synucleinmediated nerve cell toxicity in Parkinson disease and related disorders.

TITLE: Tyrosine and serine phosphorylation of alpha-synuclein have opposing effects on neurotoxicity and soluble oligomer formation

Mel B. Feany
Brigham and Women's Hospital, Boston, Massachusetts, USA.
Phone: (617) 525-4405; Fax: (617) 525-4422; E-mail:

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EDITOR'S PICK: Inhibiting the cellular process autophagy makes mice leaner

Recent data have indicated that the more brown fat cells a person has the lower their body mass. This contrasts with what is known for white fat cells, the more white fat cells a person has the greater their body mass. It has been suggested that manipulating the development of fat cells so that they become brown fat cells rather than white fat cells might be an approach to treat obesity. However, before such an approach can be developed more needs to be learned about the mechanisms regulating the formation, expansion, and interconversion of these two cell types. New research, performed by Mark Czaja and colleagues, at Albert Einstein College of Medicine, New York, has now identified a cellular process that regulates the formation of the distinct fat cell types in mice. Specifically, in mice with fat cells unable to perform the cellular process known as autophagy, there were fewer white fat cells and more brown fat cells than normal. Further, these mice were leaner than normal. The authors therefore conclude that autophagy has a critical role in determining the type of fat cell formed and suggest that this information might provide a new avenue to explore for those looking to develop therapies to treat obesity.

TITLE: Autophagy regulates adipose mass and differentiation in mice

Mark J. Czaja
Albert Einstein College of Medicine, New York, New York, USA.
Phone: (718) 430-4255; Fax: (718) 430-8975; E-mail:

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EDITOR'S PICK: Immune cells predict outcome of West Nile virus infection

Infection with West Nile virus (WNV) causes no symptoms in most people. However, it can cause fever, meningitis, and/or encephalitis. What determines the outcome of infection with WNV in different people has not been determined. But now, Philip Norris and colleagues, at the Blood Systems Research Institute, San Francisco, have found that levels of immune cells known as Tregs (immune cells that suppress the function of other immune cells) in the blood of a human or mouse infected with WNV predict whether the person or mouse will have symptoms of infection.

In the study, analysis of blood donated by 32 individuals acutely infected with WNV indicated that the frequency of Tregs increased substantially following infection. However, those individuals that were asymptomatic had higher levels of Tregs than those that exhibited symptoms of infection. Similar observations were made in mice infected with WNV. Consistent with a role for Tregs in controlling the symptoms of WNV infection, mice lacking Tregs were more susceptible to lethal infection with WNV than control mice. The authors therefore conclude that higher levels of Tregs in the blood after infection with WNV protect against severe disease in individuals with a fully functioning immune system.

TITLE: Tregs control the development of symptomatic West Nile virus infection in humans and mice

Philip J. Norris
Blood Systems Research Institute, San Francisco, California, USA.
Phone: (415) 923-5769; Fax: (415) 567-5899; E-mail:

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EDITOR'S PICK: Afib triggered by a cell that resembles a pigment-producing skin cell

The source and mechanisms underlying the abnormal heart beats that initiate atrial fibrillation (Afib), the most common type of abnormal heart beat, have not been well determined. However, a group of researchers at the University of Pennsylvania, Philadelphia, has now identified a population of cells that are like pigment producing cells in the skin (melanocytes) in the atria of the heart and pulmonary veins of mice and humans and uncovered evidence in mice that these cells contribute to Afib.

Initial analysis by the group, led by Vickas Patel and Jonathan Epstein, identified a population of cells in the atrium and pulmonary veins of mice and humans that expressed the protein DCT, which is involved in making the skin pigment melanin. Further work showed that Dct-expressing cells in the mouse heart were distinct from both heart muscle cells and skin melanocytes, although they could conduct electrical currents, which are important for coordinated contraction of the heart. Adult mice lacking Dct were susceptible to induced and spontaneous Afib and the melanocyte-like cells in their heart exhibited abnormal conduction of electrical currents in vitro. As mice lacking both melanocyte-like cells in the heart and Dct failed to develop either induced or spontaneous Afib, the authors suggest that dysfunctional melanocyte-like cells in the heart may be a trigger of Afib in humans.

TITLE: Melanocyte-like cells in the heart and pulmonary veins contribute to atrial arrhythmia triggers

Vickas Patel
University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Phone: (215) 573-8990; Fax: (215) 572-2094; E-mail:

Jonathan A. Epstein
University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Phone: (215) 898-8731; Fax: (215) 898-9871; E-mail:

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BONE BIOLOGY: Zebrafish help define how a human genetic mutation causes abnormal bone formation

TITLE: The fibrodysplasia ossificans progressiva R206H ACVR1 mutation activates BMP-independent chondrogenesis and zebrafish embryo ventralization

Eileen M. Shore
University Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 898-2331; Fax: (215) 573-2133; E-mail:

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CARDIOLOGY: Linking two distinct congenital artery malformations

TITLE: Great vessel development requires biallelic expression of Chd7 and Tbx1 in pharyngeal ectoderm in mice

Peter J. Scambler
Institute of Child Health, London, United Kingdom.
Phone: +44 20-7905-2635; Fax: +44 20-7905-2609; E-mail:

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NEPHROLOGY: 'Notch'ing up our knowledge of kidney development

TITLE: Inactivation of Notch signaling in the renal collecting duct causes nephrogenic diabetes insipidus in mice

Young-Yun Kong
Seoul National University, Seoul, Republic of Korea.
Phone: 82-2-880-2638; Fax: 82-2-872-1993; E-mail:

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HEPATOLOGY: Immune cell regulation of liver scarring

TITLE: In liver fibrosis, dendritic cells govern hepatic inflammation in mice via TNF-alpha

George Miller
New York University School of Medicine, New York, New York, USA.
Phone: (212) 263-0570; Fax: (212) 263-6840; E-mail:

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Contact: Karen Honey
Journal of Clinical Investigation

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