Such mutants included deletions of components of the CLRC histone H3K9 methyltransferase complex (clr4∆, raf1∆, and raf2∆), an HP1 protein (swi6∆), and histone deacetylases (sir2∆ and clr3∆).
In a recent study, London et al. (2007) measured apex to base repolarization gradients in genetically modified murine hearts harbouring deletions of components for Ito.
This is consistent with the phenotypic similarities between the tra1- L3733A strain and strains with deletions of components of NuA4 and SAGA, the additive effects of these mutations, and the inability of the tra1-L3733A allele to be suppressed by deletion of either hda1 or nhp10.
Similarly, deletion of components of the CDK complexes leads to severe synthetic growth defects when combined with deletion or mutation of factors involved in transcriptional elongation, including TFIIS, the Spt4/5 complex, and the CTD of RNAPII [33], [37], [39], [42] [45].
Following deletion of components of the yeast TCR apparatus, little (RAD16, MET18, RPB4; Table S1) or no (RAD7, RAD23, RAD26, RAD28, RPB9; data not shown) suppression of BRCA1-induced lethality was observed.
TCR-mediated nuclear factor kappa B (NF-κB) activation seems to be involved in differentiation of Treg cells because deletion of components of the NF-κB signaling pathway, as well as of NF-κB transcription factors, leads to markedly decreased Treg cell numbers in thymus and periphery.
In particular deletion of components of the SAGA complex, including Gcn5, confers sensitivity to CG-1521.
It is unclear why gene deletion of components of the alkaline phosphatase pathway renders cells sensitive to nickel while deletion of components of other transport pathways to the vacuole results in nickel-resistance (discussed below).
It is also unknown why deletion of components of the alkaline phosphatase pathway renders cells sensitive to nickel while deletion of components of other transport pathways to the vacuole results in nickel-resistance.
As opposed to the GPCR part of the network, deletion of components of the Ras part is lethal, as is deletion of AC or PKA.
To understand how the SCF E3 ligases regulate these cellular processes and embryonic development under in vivo physiological conditions, a number of mouse models with transgenic (Tg) expression or targeted deletion of components of SCF have been established and characterized.
