The four clusters are autonomous, dependent, linkage, and driver/independent.
These driving power and dependencies will be used in the MICMAC analysis, where the variables will be classified into four groups of autonomous, dependent, linkage, and independent (driver) variables.
(F and G ) Two models of SC-dependent linkages between sisters.
Although CR proteins are unlikely to tether sisters during wild-type meiosis, AE-dependent linkages between sisters may be a normal feature of meiosis (See Discussion).
The Rad54 paralog Tid1 is necessary to remove Scc1-dependent linkages from yeast meiotic chromosomes to facilitate normal chromosome segregation (Kateneva et al., 2005), indicating that Scc1 cohesin can tether sisters during meiosis.
The HIM-3-dependent linkages are not mediated by an SC-like structure, given that disrupting the CR protein SYP-1 only partially weakened SCC in spo-11 rec-8 double mutants, while mutations in him-3 severely abrogated SCC.
HIM-3-dependent linkages between sisters may not be essential in animals with wild-type REC-8, because REC-8-dependent SCC established during premeiotic DNA replication is likely sufficient to tether sisters until anaphase II (Severson et al., 2009).
In diplotene (our unpublished data) and diakinesis nuclei, sisters are held together by REC-8 and COH-3/4 cohesin alone, indicating that the HIM-3 and SCC-1-dependent linkages we demonstrated in pachytene are transient and are removed during late pachytene or early diplotene.
However, HIM-3-dependent linkages may prevent newly replicated sister chromatids from drifting apart in rec-8 mutants before DSBs trigger COH-3/4 to become cohesive, thus explaining the severe SCC defects observed in him-3 rec-8 double mutants with wild-type spo-11.
Here, we show that INM proceeds through the cell cycle-dependent linkage of cell-autonomous and non-autonomous mechanisms.
The large latent TGF-β complex is secreted by most cell types, including human HSC and hepatocytes [ 101, 102] and fixed in the ECM by transglutaminase-dependent linkage of latent TGF-β binding protein to fibronectin and other ECM proteins, forming a reservoir of latent TGF-β.
