Because a disruption of spindle orientation by knockdown of Cnn or EB1 causes an overproliferation phenotype similar to the one observed upon Par complex silencing, we propose that the spindle orientation defects resulting from the mislocalization of the Par complex might be responsible for the apparent overproliferation phenotype caused by Integrin knockdown.
NHS knockdown also resulted in the mislocalization of the Arp2/3 complex and disruption of the actin cytoskeleton.
Interestingly, a number of mutations identified in these genes result in the mislocalization of the protein within the cell, suggesting that their retention within the ER/GA complex is vital for the appropriate glycosylation of αDG (3).
As SDHD is one of two important subunits anchoring the SDH complex in the membrane, these two variants (G12S and H50R) may lead to a mislocalization of the complex within the mitochondrial membrane or to altering the cleavage site of signal peptide, and subsequently dysfunction of the complex.
The mislocalization of the protein may result from aberrant protein protein interactions mediated by pathologically elongated CCs (15), retaining the protein in the cytoplasm after synthesis and/or altering its physiological nucleo-cytoplasmic shuttling (67).
This cell division defect results from the mislocalization of two Tat-dependent amidases, AmiA and AmiC, which have been implicated in cleavage of the septum during cell division [52].
Despite increased mislocalization of the MSL complex, roX1 ex40 roX2Δ; D-elp1 c00296/+ male viability appears unaffected, and the viability of roX1 ex40 roX2Δ males with reduced levels of Ago2 or Loqs is also high.
Quantification of the nuclear/cytoplasmic GFP ratios from Figure 5D showed that the mislocalization of RNAPIII subunits in iwr1 Δ was statistically significant.
Mutations deleting codons for either or both Arg13 or Arg14 resulted in the mislocalization of PLN from the ER.
Mutation of both arginine residues (R10E/R12E) in the motif resulted in the mislocalization of SOAT from the ER as monitored by sucrose density fractionation.
The above studies showed that GpIbα overexpression resulted in the mislocalization of key divisional proteins from the cleavage furrow of dividing primary cells.
