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Volume 29, No. 2, Summer 2013
Buy this back issue! Available in hardcopy or as a downloadable PDF.
TABLE OF CONTENTS
ARTICLES
The Chicago Heat Parade Keeps on Marchin’ by Jim Doherty
Joe Friday on Steroids: The Life and Times of Frank Ballinger, M Squad by Jim Doherty
AUTHOR! AUTHOR!
Shaking Chicago by Robert P. Bennett
Chicago Blues by Michael Biehl
The Chi-Town Connection by Michael A. Black
Sweet Home, Chicago by Tim Chapman
Chicago? How Did I End Up Here? by Alan Cupp
The Sons of Jude by Brandt Dodson
Me, Chicago, and the Second Most Famous Detective in All of Fiction by Jim Doherty
Meet Me on Division by Barbara Fister
Chicago, Because It’s in My DNA by Jack Fredrickson
My Tenuous Chicago Connections by Kaye George
Chicago Doesn’t Let Go by Madeline (M.M.) Gornell
I Moved To Chicago for the Weather by Libby Fischer Hellmann
Chicago—Near Future and Noir: Walking Shadow by Clifford Royal Johns
Chi-hago by Kylie Logan
Mobster Chicago Used as the Colorful Back Story by Ed Lynskey
We Chicagoans by Diane Gilbert Madsen
Chicago at the Racetrack by John McEvoy
Excavating Chicago for Mysteries by Frances McNamara
When Real Life Serves as an Inspiration by Catherine O’Connell
Str
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Abstract
PTEN-induced putative kinase 1 (Pink1) is a recently identified gene linked to a recessive form of familial Parkinson's disease (PD). The kinase contains a mitochondrial localization sequence and is reported to reside, at least in part, in mitochondria. However, neither the manner by which the loss of Pink1 contributes to dopamine neuron loss nor its impact on mitochondrial function and relevance to death is clear. Here, we report that depletion of Pink1 by RNAi increased neuronal toxicity induced by MPP+. Moreover, wild-type Pink1, but not the G309D mutant linked to familial PD or an engineered kinase-dead mutant K219M, protects neurons against MPTP both in vitro and in vivo. Intriguingly, a mutant that contains a deletion of the putative mitochondrial-targeting motif was targeted to the cytoplasm but still provided protection against 1-methyl-4-phenylpyridine (MPP+)/1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced toxicity. In addition, we also show that endogenous Pink1 is localized to cytosolic as well as mitochondrial fractions. Thus, our findings indicate that Pink1 plays a functional role in the survival of neurons and that cytoplasmic targets, in addition to its other actions in the mitochondria, may be important for this protective effect.