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Mailing Address:
Patrick Emery, Ph.D
University of Massachusetts Medical School

Department of Neurobiology, LRB-726
364 Plantation Street,
Worcester, MA 01605 USA
e-mail: patrick.emery@umassmed.edu

Academic Background

Maturité scientifique. Collège Rousseau, Geneva 1987
Degree in Biology, University of Geneva 1990
Diploma in Molecular Biology,
U of Geneva Medical School
PhD, U of Geneva Medical School 1996
Postdoctoral Fellow, Brandeis University 1997-2001
Research Fellowships,
Swiss National Science Foundation

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Circadian Rhythms and their Synchronization in Drosophila

Drosophila melanogaster is a powerful model organism for understanding the genetic, molecular and neural bases of animal behaviors. Circadian rhythms are a prime example of behaviors whose molecular and neural foundations have been greatly increased by studies in Drosophila. A biological clock dictates that animals sleep and wake with a ca. 24-hour period, and this is true even when they are kept under constant conditions, without any information from the environment. Using genetic screens, many essential clock proteins (e.g. PER, TIM, figure 1) were identified in Drosophila. It has been shown that homologues of most of these proteins are also involved in generating mammalian circadian rhythms. Human homologues of Drosophila PER (hPER2) and DBT (hCK-Id) are actually mutated in patients with advanced sleep-phase syndrome. This demonstrates that the discoveries made in Drosophila are playing a crucial role in understanding human circadian behavior.

The Drosophila circadian pacemaker is a transcriptional feedback loop (fig.1), in which PER and TIM negatively regulate their own transcription.  Kinases and phosphatases determine the pace of this feedback loop by controlling PER and TIM phosphorylation, and hence their stability and repressive activity. Recent studies, including work from our lab, show that at least in circadian pacemaker neurons (the small ventral lateral neurons, fig.2) translational control of the key pacemaker protein PER is also critical for 24-hour period behavioral rhythms.  Ataxin-2 - whose mammalian homolog is involved in various neurodegenerative diseases – promotes PER translation with the help of the translational factor TYF.  A major objective of our lab is thus to understand the mechanisms by which Ataxin-2, and more generally RNA binding proteins, control circadian rhythms.   

The other major goal of our lab is to discover the mechanisms by which circadian rhythms are synchronized with the day/night cycle.  These mechanisms are critical, since the period of circadian rhythms only approximates 24 hours, and day length changes at most latitudes over the course of the year.  We are thus elucidating the cell-autonomous molecular mechanisms by which light and temperature inputs synchronize circadian molecular pacemakers.  Interestingly, it has recently become clear that communication between circadian neurons is also critical to properly synchronize circadian behavior.  Therefore, we also study the circadian neurons that detect light and temperature inputs, and determine how these neurons communicate with the rest of the circadian neural network. Our ultimate goal is to understand how different environmental inputs are integrated to optimize daily animal physiology and behavior.


Fig.1:  The circadian pacemaker is a transcriptional feedback loop.  It is synchronized with light by the intracellular photoreceptor CRY, which binds to TIM and triggers its proteasome degradation, mediated by JET. 


Fig.2:  The small ventral Lateral Neurons (left) are critical pacemaker neurons driving circadian behavior.  Knocking down ATX2 in these cells lengthen circadian behavioral rhythms to ca. 26.5 hr instead of 24hr

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