Clocks, fruit flies, and Sweden

We mentioned previously that Rosbash, Hall and Young are getting the Nobel Prize in Physiology or Medicine this year “for their discoveries of molecular mechanisms controlling the circadian rhythm”.

The Physiology/Medicine lectures were on Thursday Dec 7 at 1 pm CET (7 am Brandeis time) and are still available to view. The Biology Department enjoyed watching the lectures on “tape delay”:

From and about the winners, via Cell:

About the science and its implications:

If you need to flesh out your fantasy of going to Sweden to collect your prize, see What to expect when you’re expecting a Nobel Prize


Circadian Rhythms and When to Eat (Swedish Television)


Neuroscience Faculty Members Named AAAS Fellows

Leslie Griffith & Gina Turrigiano-2017 AAAS Fellows

Leslie Griffith (left) and Gina Turrigiano (right)

Leslie Griffith and Gina Turrigiano have been named American Association for the Advancement of Science (AAAS) Fellows for 2017. This is in recognition of their contributions and scientific leadership in the field of Neuroscience.

Leslie Griffith, Nancy Lurie Marks Professor of Neuroscience and Director of the Volen Center for Complex Systems, studies sleep and memory using Drosophila melanogaster.

Gina Turrigiano is the Joseph Levitan Professor of Vision Science. Her lab studies the mechanisms of homeostatic synaptic plasticity and their effects in developing and functioning cortex.

Vice Provost for Research Edward Hackett is also a 2017 AAAS Fellow in the Section on History and Philosophy in Science.

Griffith, Turrigiano, Hackett and the other Fellows for 2017 will be recognized on Saturday, Feb. 17, 2018 at the 2018 AAAS Annual Meeting in Austin, Texas.

Read more at BrandeisNow.

Rodal lab find surprising new link between inflammation and Lowe Syndrome

Could a disease with symptoms in the brain, eyes, and kidneys actually be caused by problems with immune cells? A team of scientists from the Rodal Lab, co-first authored by Steven Del Signore and Sarah Biber and including three Brandeis undergraduates (Katy Lehmann ‘16, Stephanie Heimler ‘17, and Ben Rosenfeld ’18), think this just might be the case with Lowe Syndrome, in a new paper published Oct 13th in PLOS Genetics.

Patients with Lowe Syndrome suffer from kidney failure, congenital cataracts, and several neurological problems including intellectual disability and seizures. Scientists have known for some time that the disease is caused by mutations in a gene called OCRL, but remain unsure how its loss causes such a diverse array of symptoms. A big problem has been that OCRL appears to do many different jobs inside cells, including controlling how they divide, how they sense their surroundings, and how they store and transport materials inside small packages called endosomes.

Fly immune cells showing the tracks of moving endosomes. Single tracks represent the path of individual endosomes over time.

To try to solve this mystery, a team of researchers from the Rodal lab used the fruit fly, which has its own version of the OCRL gene and allowed the investigators to perform powerful genetic experiments to figure out precisely what OCRL is doing, and where. To do this, the group created a fly missing its OCRL gene. They were surprised to find that, rather than eye or neurological defects, loss of OCRL hyper-activated cells of the innate immune system. The innate immune system is the first line of defense against infection in humans (and the only defense in fruit flies), when cells release inflammatory signals that mobilize specialized cells to attack invading pathogens.

The team determined that OCRL is required in one of these specialized immune cells in the fly, and that the immune-cell activation was caused by problems in a particular step of intracellular transport. Every cell of the body has its own postal service, which is used to pack and ship signals that tell the cell or its neighbors to grow, divide, or jump into action (see movie here to watch endosomes moving inside living fly immune cells). The OCRL mutant immune cells had a problem in a key step that controls whether signals get thrown in the trash or shipped outside the cell, and this caused the immune activation.

How do these findings relate to Lowe Syndrome? The authors think these results suggest a possible cause for the seizures that patients experience. When similar immune-like cells in the brain release excessive inflammatory signals, it can cause several forms of epilepsy. Further, OCRL has been linked to at least one mouse model of epilepsy. Going forward, the researchers will try to identify which immune signals are responsible, and how these findings translate to human cells.

Del Signore SJ (*), Biber SA (*), Lehmann KS, Heimler SR, Rosenfeld BH, Eskin TL, Sweeney ST, Rodal AA. dOCRL maintains immune cell quiescence by regulating endosomal traffic. Plos Genet. 2017;13(10):e1007052.



Rosbash, Hall & Young Awarded Nobel Prize

Michael Rosbash, Nobel Laureate

Brandeis researchers Michael Rosbash, the Peter Gruber Endowed Chair in Neuroscience, and Professor Emeritus of Biology Jeffrey C. Hall have received this year’s Nobel Prize in Physiology or Medicine, together with Michael Young from The Rockefeller University,  for their pioneering work on the molecular mechanisms controlling circadian rhythm.

More about Michael

More about Jeff

More about Drosophila


Sebastian Kadener Returns to Brandeis as Associate Professor

Sebastian Kadener

From 2002 to 2008, Sebastian Kadener was a postdoc working in the Michael Rosbash laboratory. He is returning to Brandeis as an Associate Professor of Biology. Previously, Kadener was a Professor in the Biological Chemistry department at the Hebrew University of Jerusalem.

The Kadener laboratory studies how molecular processes in the brain determines behavior with a special emphasis on RNA metabolism. Additionally, they study the role of circular RNAs (circRNAs) at the molecular and neural levels as well as the mechanisms underlying circadian clocks.

Kadener’s paper, “Translation of CircRNAs”, appeared in Molecular Cell in April 2017. It was reviewed in Nature Reviews Genetics and Science Daily.

Garrity lab finds moisture-sensing genes in mosquitoes

Summary figure for Garrity lab paperby Zachary Knecht, PhD candidate

As the solvent of living cells, water is critical for all life on earth.  This makes monitoring how environmental conditions impact evaporation and subsequently sensing and locating water sources important for animal survival. This is particularly critical for insects, whose small body size makes them highly susceptible to dehydration. In addition, moisture sensing, or hygrosensation, is also important for the spread of insect-born disease. Mosquitoes that spread malaria or viruses like dengue and Zika, not only need to locate bodies of standing water in which to lay eggs, but also home in on the moisture that emanates from our bodies when searching for a blood meal. This dual role for hygrosensing in mosquito biology makes their hygrosensory machinery a promising target for pest control strategies. Until now though, the genes and molecules that function in insect hygrosensation have been completely unknown.

In a pair of recent papers in the journal eLife, researchers in the Garrity Lab at Brandeis University, in collaboration with colleagues at the University of Lausanne in Switzerland, have uncovered the cellular and molecular mechanisms that underlie insect hygrosensation using the fruit fly Drosophila melanogaster. Like mosquitoes, fruit flies detect humidity through specialized, innervated hair-like structures located on their antennae called sensilla. Each hygrosensing sensilla contains one cell that responds to increasing humidity (a moist cell), and one that responds to decreasing humidity (a dry cell).  These papers demonstrate that the balance of activity between dry and moist cells allows the insect to seek out or avoid particular humidity levels, a preference which changes depending on how hydrated or dehydrated the fly is.

To identify the molecules involved in sensing moisture, the researchers looked for mutant flies unable to distinguish between humid and dry air. They found that animals with mutations in four different genes disrupted the behavior. Strikingly, each of these genes encoded a different member of the same family of sensory receptors, the so-called Ionotropic Receptors or IRs.  Although IRs are found only in invertebrates, they belong to the same family as the ionotropic Glutamate Receptors, which lie at the heart of communication between nerve cells in the animal brain, including the human brain.  IRs differ from these relatives in that instead of sensing signals sent by neurons, they detect signals coming from the environment.  IRs are best known to act as chemical receptors, but the group found that a subset of IRs act instead to sense humidity. The researchers found two broadly expressed IRs, Ir25a and Ir93a, were required by both the dry cells and moist cells while the other two IRs, Ir40a and Ir68a, were specifically required by the dry and the moist cells, respectively. This suggests that Ir25a and Ir93a contribute to the formation of both moist and dry receptors, while Ir40a and Ir68a provide the dry- and moist-specific subunits to the receptor. Consistent with this view, the loss of either Ir68a or Ir40a alone only partially reduces the animal’s ability to sense humidity, but animals with mutations in Ir25a, Ir93a or both Ir40a and Ir68a are completely blind to moisture.

Having identified the specific genes required for sensing moisture, the next step is to determine the precise mechanism by which humidity activates these receptors. Furthermore, these genes are conserved in mosquitoes and other disease vectors, providing a clear path to translate what’s known about fly hygrosensation into the mosquito. These papers lay the groundwork for new mosquito control strategies that aim to precisely inhibit their ability to seek out water to reproduce and to seek out hosts to bite and spread deadly pathogens.

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