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. 2004 Mar;9(1):4–20. doi: 10.1379/460.1

Fig 4.

Fig 4.

SBA1 suppression of AhR signaling defects and temperature sensitivity associated with the G170D mutation. (A) The HSP82 strain with (light gray bars) or without (white bars) the SBA1 expression vector, the hsp82G170D strain with (black bars) or without (dark gray bars) the SBA1 expression vector (pGal-SBA1), and the hsp82E381K strain with (horizontal lined bars) or without (hatched bars) the SBA1 expression vector (pGal-SBA1) were compared for AhR signaling. All strains carried the pTXRE5-Z reporter vector and the genomic AHR-GAL1,10-ARNT expression construct and were assayed at 32°C. (B) The YMCiG170D derivatives with the parent vector (pBevy-GU), SBA1 expression vector (pBevy-GU-SBA1), or human p23 expression vector (pBevy-GU-p23) were grown on synthetic minimal galactose medium for 3 days at the indicated temperatures. AhR, aryl hydrocarbon receptor; ARNT, aryl hydrocarbon nuclear translocator