A biocompatible supramolecular hydrogel mesh for sample stabilization in light microscopy and nanoscopy.

Most embedding media for live and fixed samples were not designed for microscopy and have issues including long polymerization times, peak of toxicity toward the sample during the sol-gel transition, and irreversibility of this transition. Gels derived from biological sources are widely used in microscopy, but their precise composition is ill-defined and can vary between batches. Non-physiological temperatures and/or specific enzymatic solutions are often needed to revert the gel back to the sol state to allow sample recovery.

Stemming Tumoral Growth: A Matter of Grotesque Organogenesis.

The earliest metazoans probably evolved from single-celled organisms which found the colonial system to be a beneficial organization. Over the course of their evolution, these primary colonial organisms increased in size, and division of labour among the cells became a remarkable feature, leading to a higher level of organization: the biological organs. Primitive metazoans were the first organisms in evolution to show organ-type structures, which set the grounds for complex organs to evolve.

Azot expression in the gut modulates organismal lifespan.

Cell Competition emerged in as an unexpected phenomenon, when confronted clones of fit unfit cells genetically induced. During the last decade, it has been shown that this mechanism is physiologically active in and higher organisms. In , Flower (Fwe) eliminates unfit cells during development, regeneration and disease states.

To fit or not to fit: death decisions from morphogen fields.

The transforming growth factor-β (TGF-β)-type morphogens are conserved throughout the animal kingdom. TGF-β-type molecules form spatial concentration gradients whose length scales with the size of growing, developing organs. Scaling of these morphogens can also be mediated by death, adjusting the size of the tissue to the range of the gradient.

A role for Flower and cell death in controlling morphogen gradient scaling.

During development, morphogen gradients encode positional information to pattern morphological structures during organogenesis. Some gradients, like that of Dpp in the fly wing, remain proportional to the size of growing organs-that is, they scale. Gradient scaling keeps morphological patterns proportioned in organs of different sizes.

Culling Less Fit Neurons Protects against Amyloid-β-Induced Brain Damage and Cognitive and Motor Decline.

Alzheimer's disease (AD) is the most common form of dementia, impairing cognitive and motor functions. One of the pathological hallmarks of AD is neuronal loss, which is not reflected in mouse models of AD. Therefore, the role of neuronal death is still uncertain.

Survival of the Fittest: Essential Roles of Cell Competition in Development, Aging, and Cancer.

Multicellular organisms evolved to resolve conflicts between individual cells, protecting the internal organization of the individual. This is illustrated by cell competition, a process that eliminates suboptimal cells from growing tissues by apoptosis. Since its early characterization in Drosophila an increasing number of conditions have been associated with competition, and mounting evidence demonstrates conservation of this process.

Elimination of unfit cells maintains tissue health and prolongs lifespan.

Viable yet damaged cells can accumulate during development and aging. Although eliminating those cells may benefit organ function, identification of this less fit cell population remains challenging. Previously, we identified a molecular mechanism, based on "fitness fingerprints" displayed on cell membranes, which allows direct fitness comparison among cells in Drosophila.

"Fitness fingerprints" mediate physiological culling of unwanted neurons in Drosophila.

Background: The flower gene has been previously linked to the elimination of slow dividing epithelial cells during development in a process known as "cell competition." During cell competition, different isoforms of the Flower protein are displayed at the cell membrane and reveal the reduced fitness of slow proliferating cells, which are therefore recognized, eliminated, and replaced by their normally dividing neighbors. This mechanism acts as a "cell quality" control in proliferating tissues.