Endogenous bioluminescent reporters reveal a sustained increase in utrophin gene expression upon EZH2 and ERK1/2 inhibition.

Duchenne muscular dystrophy (DMD) is an X-linked disorder caused by loss of function mutations in the dystrophin gene (Dmd), resulting in progressive muscle weakening. Here we modelled the longitudinal expression of endogenous Dmd, and its paralogue Utrn, in mice and in myoblasts by generating bespoke bioluminescent gene reporters. As utrophin can partially compensate for Dmd-deficiency, these reporters were used as tools to ask whether chromatin-modifying drugs can enhance Utrn expression in developing muscle.

Oncogenic Rag GTPase signaling enhances B cell activation and drives follicular lymphoma sensitive to pharmacological inhibition of mTOR.

The humoral immune response demands that B cells undergo a sudden anabolic shift and high cellular nutrient levels which are required to sustain the subsequent proliferative burst. Follicular lymphoma (FL) originates from B cells that have participated in the humoral response, and 15% of FL samples harbor point, activating mutations in , an essential activator of mTORC1 downstream of the sensing of cellular nutrients. The impact of recurrent mutations in B cell function and lymphoma is unexplored.

Is the avian glycogen body a secretory organ?

In the present study we have observed with the electron microscope the glycogen body of the chick, Gallus domesticus, which constitutes a spinal cord circumventricular organ specific of birds. We have detected in young chickens and embryos the presence of considerable amounts of glycogen particles in the cerebrospinal and vascular compartments, coming from the glycogen body cells, which are able to discharge part of their glycogen into either the central canal or the capillary lumen, via ependymal and endothelial cells respectively. If this secretion is a physiological condition, we propose that the glycogen body would play a role in the maintenance of the hydric and glucose haemostasia in the central nervous system, as well as in the osmoregulation.

Glial fibrillary acidic (GFA) protein in rat spinal cord. An immunoperoxidase study in semithin sections.

The distribution of glial fibrillary acidic (GFA) protein was examined in cervical spinal cord of adult rat, according to the immunocytochemical peroxidase-antiperoxidase (PAP) method in semithin sections (1-2 microns). We have found astroglial cells in proximal regions of both ventral and dorsal roots. The presence of astrocytic processes reaching the central canal, only in the dorsal region suggest that they are the only radial glia cells which remain attached to the central canal.

Glial fibrillary acidic protein (GFAP) in spinal cord of postnatal rat. An immunoperoxidase study in semithin sections.

The presence and distribution of gliofibrillary acidic protein (GFAP) was studied in the postnatal spinal cord of the rat. On birth GFAP can be seen in astrocytic bodies and their processes of ventral columns; perivascular glial membrane was initially seen within white and gray matter; most of the fibers were transversally oriented. There are many mitotic cells, some of them with GFAP in their cytoplasm, while others lack it, thus providing strong evidence to identify two cellular populations as astrocytes and, possibly, oligodendrocytes and to state that neuroglial cells differentiate to astrocytes before myelination gliosis.