Molecular, Cellular, and Developmental Biology at the University of Michigan
Molecular, Cellular, and Developmental Biology
Molecular, Cellular, and Developmental Biology

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Linda Barthel of the Raymond Lab.
Members of the Chapman Lab.
Michael O'Connor of the Chapman Lab.
Members of the Jakob Lab.

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The Department of Molecular, Cellular and Developmental Biology strives to develop new knowledge through basic research about the function of living organisms with focus on the molecular and cellular levels of all branches of life - bacteria, plants, and animals. Our faculty research strengths are animal physiology and neurobiology, biochemistry, cell biology, developmental biology, microbiology and plant molecular biology. We are home to the undergraduate concentration in Cell and Molecular Biology that graduates nearly 200 students per year. Our General Public and Pre-College Students section offers answers to questions about biology. We hope you find our site informative!
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MCDB News
Undergraduates
and their faculty adviser, Ray Barbehenn, helped explain an observation that had puzzled insect ecologists who study gypsy moth caterpillars. Read more.

MCDB News
Elaina Breznau,
a graduate student in the Miller Lab, was recently awarded a Journal of Cell Science Travelling Fellowship. Read more.

MCDB News
Lilia Popova,
a member of the Schiefelbein Lab, has been selected as a 2013 Intel Science Talent Search Finalist. Read more.

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MCDB Professors
James Bardwell, Jianming Li, and Eran Pichersky have been named American Association for the Advancement of Science (AAAS) Fellows. Read more.

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Adnan Syed,
a PhD student in the Boles Lab, was recently awarded an American Heart Association Predoctoral Fellowship. Read more.

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Professor Emeritus
Sally Allen
passed away November 13, 2012 at age 86 after a brief illness. Sally was professor of biology for over 30 years and was a tireless and dedicated researcher and lecturer. Read more.

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Lipid storage disorders block lysosomal trafficking by inhibiting a TRP channel and lysosomal calcium release
Nature Communications 3, Article number: 731 doi:10.1038/ncomms1735, 13 March 2012
Dongbiao Shen, Xiang Wang, Xinran Li, Xiaoli Zhang, Zepeng Yao, Shannon Dibble, Xian-ping Dong, Ting Yu, Andrew P. Lieberman, Hollis D. Showalter and Haoxing Xu

Lysosomal lipid accumulation, defects in membrane trafficking and altered Ca2+ homoeostasis are common features in many lysosomal storage diseases. Mucolipin transient receptor potential channel 1 (TRPML1) is the principle Ca2+ channel in the lysosome. Here we show that TRPML1-mediated lysosomal Ca2+ release, measured using a genetically encoded Ca2+ indicator (GCaMP3) attached directly to TRPML1 and elicited by a potent membrane-permeable synthetic agonist, is dramatically reduced in Niemann-Pick (NP) disease cells. Sphingomyelins (SMs) are plasma membrane lipids that undergo sphingomyelinase (SMase)-mediated hydrolysis in the lysosomes of normal cells, but accumulate distinctively in lysosomes of NP cells. Patch-clamp analyses revealed that TRPML1 channel activity is inhibited by SMs, but potentiated by SMases. In NP-type C cells, increasing TRPML1's expression or activity was sufficient to correct the trafficking defects and reduce lysosome storage and cholesterol accumulation. We propose that abnormal accumulation of luminal lipids causes secondary lysosome storage by blocking TRPML1- and Ca2+-dependent lysosomal trafficking.

This paper was featured in the U-M News Service article "U-M biologists find potential drug that speeds cellular recycling."

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