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Tuesday, September 13th 2016 - 11 a.m.
Dr Jean-Charles Lambert

From GWAS to biology: towards a better understanding of Alzheimer's disease

Phd Programme

Breakdance in mammalian heterochromatin!

Super-resolution image depicting DNA Double Strand Breaks (revealed by g-H2AX, the main DSB marker, in red) in centromeres (in green), localized around the DAPI-dense regions corresponding to pericentromeres.

July 7, 2016

The teams of Evi Soutoglou and Bernardo Reina-San-Martin have taken advantage of the CRISPR/Cas9 genome editing technology to identify the molecular mechanisms regulating the repair of double stranded DNA breaks (DSBs) arising in highly compacted chromatin (constitutive heterochromatin). These results are published on July 7th 2016 in Molecular Cell.



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Cell division: how molecular motors team up for separating cells

Cells are placed vertically in micro-fabricated cavities; cytokinetic rings of yeasts (schematically at the top) and mammalian cells (schematically at the bottom) are visible (yellow and green rings respectively). These structures are characterized by distinct collective dynamic of molecular motors.


© IGBMC / Team Daniel Riveline

July 1, 2016

The team of Daniel Riveline at IGBMC (CNRS, INSERM, University of Strasbourg) and at the Institute of Science and Supramolecular Engineering (ISIS, CNRS, University of Strasbourg), in collaboration with the team of Karsten Kruse (Saarland University, Germany) has revealed the mechanisms leading to physical separations of yeast and mammalian cells. These results are published in the journal Nature Communications, July 1st 2016.

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Fragile-X Syndrome: one more step to finding a cure for this disease

Under normal condition (left), FMRP helps produce the Dgkk enzyme in neurons. In the fragile X situation, in the absence of FMRP (right), Dgkk is not sufficiently produced. Acting on Dgk enzymatic activity would be a way to correct the defects associated with the fragile X syndrome.
© IGBMC / Hervé Moine

July 11, 2016

A study supervised by Hervé Moine evidenced a pathogenic mechanism for fragile X syndrome. This genetic disease most often causes intellectual disabilities, behavioral problems and physical abnormalities. These results were published in the Proceedings of the National Academy of Sciences (PNAS) on May 27th.


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The formation of heart valves finally determined

Picture of the endocardial cells of zebrafish heart after photoconversion(1) of the ventricle of the heart. The ventricle which is photoconverted appears in mauve while the atrium, which is not photoconverted, appears in green. This approach allowed the researchers to address cellular mechanisms associated with the formation of the heart valves.


(1) Photoconversion: the conversion of a substance from one form to another by using the energy supplied by light.

May 25, 2016

The team of Julien Vermot is working on the mechanisms that regulate the formation of the heart valves. The researchers were able to show how heart valves are formed in response to changes in the extracellular matrix that is mediated by mechanical forces exerted by the heart muscle contractions. The researchers hope this discovery will help to better understand how to grow the heart valves in vitro. These results have been published on May 25, 2016 in the journal Nature Communications.


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