The human factor showed very strong complementation, almost to the wild type level, whereas E. coli IF3 had a weak, but detectable activity.
One meiotic mutant that was not included in the initial complementation testing is hdm, as all strong complementation groups were accounted for by mei-217, mei-218, mei-9, and nod, and the two novel complementation groups that show the highest level of nondisjunction do not map to hdm (data not shown).
Moreover, it turns out that if the stronger Complementation axiom (P.6) holds, then all of these principles are trivially satisfied in any domain in which there is a universal entity: in that case, regardless of ξ, the sum of any two entities is just the complement of the difference between the complement of one minus the other.
These findings suggest that the affinity of the protein protein interaction used for library construction contributes to protein-fragment complementation because the higher affinity interaction (IAAL-E3/IAAL-K3) consistentlyieldeded stronger complementation with the fragmented IFP.
This combinatorial approach has the advantage that it samples all of the possible designs for constructing fragmented proteins and provides information on the backbone fission sites that yield fragments with the strongest functional complementation.
The IGF1 involved pathways such as "PI3K-Akt signaling", "HIF-1 signaling", "mTOR signaling ", "Focal adhesion" and "Progesterone-mediated oocyte maturation", are all present in Luminal-B driver pathway collaboration, and 3 of them are even Luminal-B specific driver pathways, which is a strong support and complementation for our current understandings of ER + subtype, especially Luminal-B.
Complementation was strong at positions 28 and 58, moderate at position 69, and too weak to be detected at positions 16 and 91.
Complementation was stronger in cells expressing GN-link-aSyn and aSyn-GC than in cells expressing aSyn-GN and aSyn-GC, supporting an antiparallel interaction between two aSyn molecules (Table 1 and Fig. 1A F).
Transheterozygous combinations with cheerio and chic revealed strong second site non-complementation for the cheerio and chic phenotypes of irregular organization of cortical F-actin and second site non-complementation or even enhancement of their delayed BC migration phenotype (Fig. 7A,B).
Knocking out the kinase YbdM did not provoke strong phenotypes, possibly due to complementation of its function by remaining Hanks kinases.
In minimal media, these additional N-glycans are only observed if AfOch1 is expressed from the strong gpdA promoter of the complementation construct.
