CTCF and CTCFL in cancer.

CTCF plays a key role in organizing chromatin into TAD structures but it can also function as a transcription factor. CTCFL (CTCF-like), the paralog of CTCF, is normally transiently expressed in pre-meiotic male germ cells together with ubiquitously expressed CTCF. It plays a unique role in spermatogenesis by regulating expression of testis-specific genes. Genetic alterations in CTCF and its paralog CTCFL have both been found in numerous cancers, but it remains unknown to what extent CTCFL deregulates transcription on its own or by opposing CTCF. Here, we discuss some of the potential mechanisms by which these two proteins could alter gene regulation and contribute to oncogenic transcriptional programs.

A conserved mechanism drives partition complex assembly on bacterial chromosomes and plasmids.

Chromosome and plasmid segregation in bacteria are mostly driven by ParABS systems. These DNA partitioning machineries rely on large nucleoprotein complexes assembled on centromere sites (parS). However, the mechanism of how a few parS-bound ParB proteins nucleate the formation of highly concentrated ParB clusters remains unclear despite several proposed physico-mathematical models. We discriminated between these different models by varying some key parameters in vivo using the F plasmid partition system. We found that "Nucleation & caging" is the only coherent model recapitulating in vivo data. We also showed that the stochastic self-assembly of partition complexes (i) is a robust mechanism, (ii) does not directly involve ParA ATPase, (iii) results in a dynamic structure of discrete size independent of ParB concentration, and (iv) is not perturbed by active transcription but is by protein complexes. We refined the "Nucleation & caging" model and successfully applied it to the chromosomally encoded Par system of Vibrio cholerae, indicating that this stochastic self-assembly mechanism is widely conserved from plasmids to chromosomes.