In vitro incorporation of14C labeled precursors into swine coronary arterial phospholipids

Zusammenfassung Der Grad des Einbaus von¹⁴C-markierten Prekursoren in die Arterienphospholipide des Schweins war folgender: Cholin>Aethanolin>Serin> Glycerin>Format>Azetat. Bei Bebrütung von Arterien mit¹⁴C-Cholin oder¹⁴C-Aethanolamin trat ein deutlich erhöhter Einbau von¹⁴C in das Phosphatidylcholin auf.

---

---

This investigation was supported by Grant No. 5R01-HE10172-03 from the National Heart Institute, U.S.P.H.S.     

The DNA double-strand “breakome” of mouse spermatids

De novo germline mutations arise preferentially in male owing to fundamental differences between spermatogenesis and oogenesis. Post-meiotic chromatin remodeling in spermatids results in the elimination of most of the nucleosomal supercoiling and is characterized by transient DNA fragmentation. Using three alternative methods, DNA from sorted populations of mouse spermatids was used to confirm that double-strand breaks (DSB) are created in elongating spermatids and repaired at later steps. Specific capture of DSB was used for whole-genome mapping of DSB hotspots (breakome) for each population of differentiating spermatids. Hotspots are observed preferentially within introns and repeated sequences hence are more prevalent in the Y chromosome. When hotspots arise within genes, those involved in neurodevelopmental pathways become preferentially targeted reaching a high level of significance. Given the non-templated DNA repair in haploid spermatids, transient DSBs formation may, therefore, represent an important component of the male mutation bias and the etiology of neurological disorders, adding to the genetic variation provided by meiosis.     

The behavioral effects of 2,5-dimethoxy-4-alkyl amphetamines

Cellular and Molecular Life Sciences - Le comportement des rats a été fortement influencé par des dérivés de la 2,5-diméthoxyamphétamine Le mécanisme...     

Identification of mutations in CUL7 in 3-M syndrome

Intrauterine growth retardation is caused by maternal, fetal or placental factors that result in impaired endovascular trophoblast invasion and reduced placental perfusion. Although various causes of intrauterine growth retardation have been identified, most cases remain unexplained. Studying 29 families with 3-M syndrome (OMIM 273750), an autosomal recessive condition characterized by severe pre- and postnatal growth retardation, we first mapped the underlying gene to chromosome 6p21.1 and then identified 25 distinct mutations in the gene cullin 7 (CUL7). CUL7 assembles an E3 ubiquitin ligase complex containing Skp1, Fbx29 (also called Fbw8) and ROC1 and promotes ubiquitination. Using deletion analysis, we found that CUL7 uses its central region to interact with the Skp1-Fbx29 heterodimer. Functional studies indicated that the 3-M-associated CUL7 nonsense and missense mutations R1445X and H1464P, respectively, render CUL7 deficient in recruiting ROC1. These results suggest that impaired ubiquitination may have a role in the pathogenesis of intrauterine growth retardation in humans.