Ink flow patterns and histological analysis suggested that AVMs in Notch and TGFβ mutants involved a shunting of blood from the DA into the ACV and CCV [6], [60], [61], [62], [63].
Here, we show that disruption of epithelial barrier function by Tir-negative mutants involves an initial lag period, which provides an explanation of why previous reports have failed to observe the barrier-disrupting capacity of the tir mutant.
The H300N mutant involves a substantial perturbation of the active site, so it was fortunate that we could solve this crystal structure.
Many MIDY mutants involve gain or loss of a cysteinyl residue [4], [5], [6], [7], [8], and proinsulin-C(A7)Y (causing diabetes in the Akita mouse) is the most studied of these [15], [23], [33], [34], [35], [36].
Cx32-E186K altersurfacecelectrostaticic potential in an exactly similar way as Cx50-E201K since both mutants involve the same residue substitution.
Most of these mutants involve residues that are conserved.
The signalling cascades triggered by the Met2P and Met2S specificity-switch mutants involve distinct, non-equivalent mechanisms [ 9].
Molecular defects in five such mutants involve genes encoding mitochondrial ribosomal protein (CG7925), ADP/ATP translocase (CG16944), the citrate synthase (CG3861), an ethanolamine kinase (CG3525), and an aminopeptidase (CG5518).
To obtain more mutants involving acetate repression, a third screen was carried out using a pyrG89;areA217;facA700 strain and the same selection process.
Given that most of the variation in DNA methylation was fairly mild (max ∼10%) we consider it unlikely that they cause largescale changes in chromatin organization, especially when one considers that very few null mutants involved in DNA methylation (with a few notable exceptions such as mom1, ddm1 and met1) seem to affect chromatin compaction.
