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. Author manuscript; available in PMC: 2010 Jun 25.
Published in final edited form as: J Biol Chem. 2007 Nov 28;283(4):1962–1973. doi: 10.1074/jbc.M706877200

FIGURE 6. SED1 overexpression suppresses the drug sensitivity and SLN1-SKN7 pathway activation phenotypes of a ccw12 mutant.

FIGURE 6

A, growth of the ccw12Δ mutant strain, JF2278 carrying a CEN-based (pHJ1604) or 2-μm based (pHJ1606) SED1 expression plasmid, was assayed on YPD plates or YPD plates containing 25 μg/ml HB, 30 μg/ml Congo Red (CR), or 20 μg/ml CFW. The same strain carrying a complementing CCW12 plasmid (pSS1559) or empty vector (pRS313) is shown for comparison. SLN1-SKN7 pathway activation was measured using the POCH1-lacZ reporter, pZL1320 (10). β-Galactosidase (β-gal) activity values are the average of three of more transformants and are represented in Miller units normalized to protein. Standard deviations (SD) are shown in parentheses. B, SED1 contributes to cell wall integrity of log phase cells in the absence of Ccw12p. Wild type (WT) (JF1565), sed1Δ (JF2337), ccw12Δ (JF2278), and ccw12Δsed1Δ (JF2338) strains carrying the POCH1-lacZ reporter, pZL1320 (10), were grown selectively, diluted into YPD media, and spotted on YPD plates containing 0 (YPD) or 15 mg/ml HB. β-Galactosidase activity is the average of three of more transformants and is represented in Miller units and normalized to protein concentrations. Standard deviations are shown in parentheses.