Mammalian p21-activated kinase 1 (Pak1) is a highly conserved effector for the small GTPases Cdc42 and Rac1 [1]. In lower eukaryotes, Pak1 homologs are regulated during the cell cycle by phosphorylation. Here, we show that Pak1 is phosphorylated during mitosis in mammalian fibroblasts. This phosphorylation occurs at a single site, Thr 212, within a domain that is unique to Pak1. Cdc2 phosphorylates Pak1 at the identical site in vitro, and inhibition of Cdc2 abolishes Pak1 mitotic phosphorylation in vivo, indicating that Cdc2 is the kinase responsible for phosphorylating Pak1 in mitotic cells. Expression of a Pak1 mutant in which Thr 212 is replaced with a phosphomimic (aspartic acid) has marked effects on the rate and extent of postmitotic spreading of fibroblasts. The mitotic phosphorylation of Pak1 does not alter the basal or Rac-stimulated activity of this kinase, but it does affect the coimmunoprecipitation of at least three proteins with Pak1. These findings are the first to implicate a mammalian Pak in cell cycle regulation and suggest that Pakl, as a result of phosphorylation by Cdc2, alters its association with binding partners and/or substrates that are relevant to the morphologic changes associated with cell division.

The authors present a new study on 789 cases of congenital thoracic malformations including 638 pectus excavatum and 151 Poland syndromes, according to a new classification which completes Chin's one. All these malformations were treated with silicone elastomer implants. The contribution of computer-aided design and manufacturing (CAD/CAM) since 2008 is essential. The one-stage surgical protocol is precisely described. The results are impressive, permanent, for life, and complications are rare. The authors evoke a common vascular etiopathogenesis theory at the embryonic stage and question the heavy techniques of invasive remodeling that are most often unjustified.

La technique des implants sur mesure 3D en élastomère de silicone, permet à partir d’un scanner de combler avec précision, une malformation thoracique congénitale, qu’elle soit osseuse (pectus excavatum) ou musculaire (Syndrome de Poland) avec pour conséquence un repositionnement naturel des seins. Nous rapportons notre expérience de 25 ans chez 301 femmes (234 Pectus et 64 Poland). La correction pariétale doit être faite en première intention. Il est fréquent de devoir réaliser dans un second temps chez la femme, une plastie mammaire complémentaire notamment en présence d’une insuffisance de volume glandulaire ou d’un sein tubéreux assez fréquemment associé.

Mitochondrial protein import follows a general pathway for preproteins with amino-terminal presequences. The discovery of novel import components has now revealed a distinct pathway for translocation of hydrophobic proteins across the intermembrane space and into the inner membrane.