4 research outputs found

    Beyond Mutexes, Semaphores, and Critical Sections

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    International audienceThe traditional approach to multitasking synchronization has been to use Mutexes, Semaphores, and Critical sections. However, those primitives can lead to inefficiency or, even worse, to error conditions such as, for example, dead or live locks or priority inversion. The problems with those primitive are particularly vivid with real-time systems. Also, with the rapid deployment of multi-core systems, those traditional mechanisms are showing new classes of issues. This talk will discuss how the use of non-blocking algorithms through atomic and barrier operations can lead to more robust, deterministic and higher performance systems

    X-linked primary ciliary dyskinesia due to mutations in the cytoplasmic axonemal dynein assembly factor PIH1D3

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    By moving essential body fluids and molecules, motile cilia and flagella govern respiratory mucociliary clearance, laterality determination and the transport of gametes and cerebrospinal fluid. Primary ciliary dyskinesia (PCD) is an autosomal recessive disorder frequently caused by non-assembly of dynein arm motors into cilia and flagella axonemes. Before their import into cilia and flagella, multi-subunit axonemal dynein arms are thought to be stabilized and pre-assembled in the cytoplasm through a DNAAF2–DNAAF4–HSP90 complex akin to the HSP90 co-chaperone R2TP complex. Here, we demonstrate that large genomic deletions as well as point mutations involving PIH1D3 are responsible for an X-linked form of PCD causing disruption of early axonemal dynein assembly. We propose that PIH1D3, a protein that emerges as a new player of the cytoplasmic pre-assembly pathway, is part of a complementary conserved R2TP-like HSP90 co-chaperone complex, the loss of which affects assembly of a subset of inner arm dyneins
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