Category:Team Sandy Konas

Fig 5E, Interestingly, mutation of dhp1 does not reduce this histone modification at the same region (Fig 5E), suggesting that Dhp1 plays a role in effective maintenance of epigenetic silencing downstream of H3K9me.

Figure 2

Figure 1E

Figure 5

Figure 3J & 3K show that transfection with the SIRT3 expression construct significantly reduces hydrogen peroxide-induced apoptosis by enhancing antioxidant activity of CAT and MnSOD

Figure 2(E-F) shows that pSIRT3 transfection increases gene & protein levels of MnSOD. 2G indicates enzymatic activity of MnSOD is also enhanced.

Figure 2(H-I) shows that pSIRT3 transfection increases gene & protein levels of CAT. 2J indicates enzymatic activity of CAT is also enhanced.

Figure 1E

Fig 1C

Figure 1A

Figure 2B&C show that levels of H3K9me2 at the reporter genes embedded in these regions were substantially reduced at these loci in cells deficient in dhp1

Fig 2 B & C shows that levels of H3K9me2 at the reporter genes embedded in these regions were substantially reduced at these loci in cells deficient in dhp1

Figure 2A

Figure 2A chromosome segregation defects in dhp1-1 mutants and Supp. 5

Figure 1B,C Similar to clr4Δ, dhp1-1 but not din1-null (din1Δ) cells form white colonies, indicating a silencing defect at the mating type locus unique to the dhp1 mutant.

Figure 1B,C dhp1-1 but not din1-null (din1Δ) cells form white colonies, indicating a silencing defect at the mating type locus unique to the dhp1 mutant

Figure 2 Since Ckb1 is a regulatory subunit of casein kinase II (CK2) CK2 phosphorylates Swi6

silencing defects in ckb1Δ cells was comparable with that caused by disruption of other heterochromatic genes, swi6 (Fig. 1B).

silencing defects in ckb1Δ cells was comparable with that caused by disruption of other heterochromatic genes, including clr3, (Fig. 1B).

silencing defects in ckb1Δ cells was comparable with that caused by disruption of other heterochromatic genes, including clr4,Fig. 1B).

disruption of ckb1 alleviated the silencing of marker genes inserted in centromeric heterochromatin (Fig. 1B)

We verified the localization of the fusion protein by

fluorescence microscopy and found it to be present mainly in the nuclear membrane (Fig. 1A)

Figure 1C Quantitative analysis by RT-qPCR revealed that lem2Δ cells display a twofold increase in reporter gene expression

needs relation

Figure 5

Figure 6 this protein is keeping csh3 in the right place

Figure 6. Following transformation, Csh3-GFP localized to the cytoplasm,

Figure 6 Cap1-GFP localized to cortical patches at the growing ends or septum

Figure 7 actin patches were not properly formed in cap1Δ

Figure 7

Figure 4

Figure 2

ChIP–chip analysis of the genome-wide distribution of Sgo2-Flag in logarithmically growing wt cells. It is noteworthy that the probes used in the tiling array did not encompass regions outside the rDNA repeats on chromosome 3. (c) Magnification of the ChIP–chip data for the subtelomeric regions shown in b.