Microperoxisomes in steroidogenic cells of the rat ovary: Interstitial,thecal and luteal cells

Summary Microperoxisomes are present in luteal, interstitial and thecal cells. They are in close relation with smooth endoplasmic reticulum and lipids. Their probable role in steroid biosynthesis is discussed.This work was supported by funds from CNR (Contract N.CT-77.01921.4).     

Molecular and Cellular Basis of Regeneration and Tissue Repair

Tissue repair and regeneration are very complex biological events, whose successful attainment requires far more than mere cell division. However, almost unavoidably they entail cell proliferation as a fundamental premise. Full regeneration or repair cannot be achieved without replacing cells lost to disease or injury, replacement that can only take place via proliferation of surviving cells. This review endeavors to outline the molecular bases of exit from and reentry into the cell cycle. In recent years, the decision to proliferate or not has been seen as mostly the concern of cyclins and cyclin-dependent kinases. This account tries to show that cell cycle inhibitors are as important as the positive regulators in the making of this decision. Finally, the authors wish to suggest that the molecular knowledge of the cell cycle can be harnessed to the benefit of many aspects of regenerative medicine.     

Microperoxisomes in steroidogenic cells of the rat ovary: interstitial, thecal and luteal cells

Microperoxisomes are present in luteal, interstitial and thecal cells. They are in close relation with smooth endoplasmic reticulum and lipids. Their probable role in steroid biosynthesis is discussed.     

Replication fork recovery and regulation of common fragile sites stability

The acquisition of genomic instability is a triggering factor in cancer development, and common fragile sites (CFS) are the preferential target of chromosomal instability under conditions of replicative stress in the human genome. Although the mechanisms leading to CFS expression and the cellular factors required to suppress CFS instability remain largely undefined, it is clear that DNA becomes more susceptible to breakage when replication is impaired. The models proposed so far to explain how CFS instability arises imply that replication fork progression along these regions is perturbed due to intrinsic features of fragile sites and events that directly affect DNA replication. The observation that proteins implicated in the safe recovery of stalled forks or in engaging recombination at collapsed forks increase CFS expression when downregulated or mutated suggests that the stabilization and recovery of perturbed replication forks are crucial to guarantee CFS integrity.