Cellular basis of limb morphogenesis.

How the size and shape of developing tissues is encoded in the genome has been a longstanding riddle for biologists. Constituent cells integrate several genetic and mechanical signals to decide whether to divide, die, change shape or position. We review here how morphogenetic cell behaviors contribute to leg formation from imaginal disc epithelia in the insect Drosophila melanogaster, as well as to direct embryonic limb outgrowths in the non-insect pancrustacean Parhyale hawaiensis. Considering the deep conservation of developmental programs for limb patterning among arthropods and other bilaterians, moving forward, it will be exciting to see how these genetic similarities reflect at the cellular and tissue mechanics level.

mRNA decapping is an evolutionarily conserved modulator of neuroendocrine signaling that controls development and ageing.

Eukaryotic 5'-3' mRNA decay plays important roles during development and in response to stress, regulating gene expression post-transcriptionally. In Caenorhabditis elegans, deficiency of DCAP-1/DCP1, the essential co-factor of the major cytoplasmic mRNA decapping enzyme, impacts normal development, stress survival and ageing. Here, we show that overexpression of dcap-1 in neurons of worms is sufficient to increase lifespan through the function of the insulin/IGF-like signaling and its effector DAF-16/FOXO transcription factor. Neuronal DCAP-1 affects basal levels of INS-7, an ageing-related insulin-like peptide, which acts in the intestine to determine lifespan. Short-lived dcap-1 mutants exhibit a neurosecretion-dependent upregulation of intestinal ins-7 transcription, and diminished nuclear localization of DAF-16/FOXO. Moreover, neuronal overexpression of DCP1 in Drosophila melanogaster confers longevity in adults, while neuronal DCP1 deficiency shortens lifespan and affects wing morphogenesis, cell non-autonomously. Our genetic analysis in two model-organisms suggests a critical and conserved function of DCAP-1/DCP1 in developmental events and lifespan modulation.

Fracture of femoral component in a resurfacing total knee arthroplasty.

We present a case of an unusual complication after a resurfacing total knee arthroplasty. Fracture of the uncemented porous-coated femoral component occurred 4 years after its implantation. The mechanical axis was restored and collateral ligament balance was achieved at the primary procedure. At revision, the femoral component was found fractured at the junction of the trochlea with the medial condyle, anteriorly to the medial peg. A thin layer of fibrous tissue was interposed between bone and metal under the fracture area. Metallurgical analysis of the fractured component revealed fatigue failure but no structural defect. Lack of bony support and excessive cyclic loading led to fracture of the implant.