Awardees' Articles

HFSP Young Investigator Grant holder Richard Benton and colleagues

Tuesday 6th December 2016

Pseudogenes are widely considered to be non-functional parts of the genome. New work has uncovered the phenomenon of pseudo-pseudogenes in the olfactory receptor repertoires of drosophilids that encode for functional receptor proteins through neuron-specific read-through of premature termination codons.

 

HFSP Young Investigator Grant holder Giuliano Scarcelli and colleagues

Monday 5th December 2016

Mechanical properties, such as stiffness, promise to provide new biomarkers and diagnostic indicators for underlying disease of biological organisms, from cells to organs. However, existing technology is invasive and/or too slow to provide mechanical information of large samples at high resolution. A new optical configuration that speeds up the acquisition by ~100 times is described below.

 

HFSP Young Investigator Grant holder Utpal Bhadra and colleagues

Friday 2nd December 2016

The loss of the entire X chromosome in Drosophila results in a genome-wide aneuploid effect. During evolution, this effect drifted gradually from the X-chromosomes to the autosomes in a wide range of species, which depicts that transacting regulatory modifiers counteract their targets in two separate chromosomes. These modifiers are hyper-activated in dosage compensated males and eventually mitigate inverse aneuploid effects for maintaining the equality in autosomal target gene expression in both...

 

HFSP Long-Term Fellow Marieke Scholvinck

Monday 28th November 2016

The brain is never idle. Even when we do nothing, during sleep for instance, it is very active. This activity displays a certain structure, and how this arises is not known. We have now shown this structure to obey well-known brain anatomical principles.

 

HFSP Long-Term Fellow Paola Tognini and colleagues

Friday 25th November 2016

Signals from the gut microbiota participate in the maintenance of host metabolic homeostasis. A new investigation reveals the molecular mechanism underlying the effect of diet-dependent gut flora dysbiosis on the induction of circadian gene transcription in the liver.

 

HFSP Career Development Award holder Hervé Seitz and colleagues

Thursday 24th November 2016

microRNAs interact with many mRNAs through conserved binding sites, and are therefore believed to control more than 60% of mammalian coding genes. But various biases in current experimental and computational methods generate high rates of false positives: many published microRNA/mRNA interactions are thus likely to be biologically inconsequential.

 

HFSP Long-Term Fellow Timothy Hore and colleagues

Tuesday 22nd November 2016

Vitamins A and C can enhance success in the challenging process of converting adult cells into stem cells. We report that the way these vitamins complement each other to do this is by erasing 'epigenetic memory' associated with DNA, which could help improve technologies geared towards regenerative medicine and stem cell therapy.

 

HFSP Program Grant holder Laurent Blanchoin and HFSP Young Investigator Grant holders Maxence Nachury and Manuel Théry and colleagues

Friday 18th November 2016

Microtubules are rigid filament components of the cytoskeleton. They are continuously regenerating and have a half-life of only a few minutes. Microtubules grow steadily from the centre of the cell towards the periphery but can randomly disassemble at any moment.

 

HFSP Long-Term Fellow Yonatan Stelzer and colleagues

Wednesday 16th November 2016

In mammals, parent-specific DNA methylation marks are required to control the parent-of-origin expression of imprinted genes. Disruption of these marks results in a variety of phenotypes, ranging from early embryonic lethality to neurodegenerative syndromes and cancer.

 

HFSP Long-Term Fellow Marcus Wilson and colleagues

Tuesday 8th November 2016

DNA is under constant attack, which can cause unwanted genetic mutations and cancer. Luckily, our cells have a host of DNA repair proteins, which help to fix most of the damage. A new study takes a look at how 53BP1, a key DNA repair protein, is recruited to sites of DNA breaks.