Table I.

Mutants employed and their characteristics

L^S, No growth at 80 μE m⁻² s⁻¹; HL^S, no growth at 500 μE m⁻² s⁻¹; R, light resistant, i.e. growth at 500 μE m⁻² s⁻¹; cont., continued; WT, wild type; ND, not done.

Mutant	Phenotypes			Mutational Defect	Reference
		Growth without Acetate	Light Sensitivity			Fluorescence Induction
ΔpetA	−	LS	Cont. rise to Fmax	Deletion of chloroplast petA gene	Kuras and Wollman (1994)
mcd1-F16	−	LS	Cont. rise to Fmax	Defect in a nuclear gene that controls petD mRNA stability	Drager et al. (1998)
tca1-693	−	LS	Cont. rise to Fmax	Nuclear gene; encodes a translation activator for petA mRNA	Wostrikoff et al. (2001)
petD-PWYE	−	LS	Cont. rise to Fmax	A petD mutation that alters the QO pocket of the cytb6/f complex	Zito et al. (1999)
clpP1-AUU	+	R	WT	Mutation in clpP1 start codon resulting in low ClpP protease level	Majeran et al. (2000)
petC-Δ1 clpP1-AUU	−	LS	ND	2-bp deletion in PETC; devoid of Rieske protein	Majeran et al. (2000)
P1-15	−	HLS	Cont. rise to Fmax	Nuclear mutation	Dent et al. (2005) and this report
P2-26	−	LS	Cont. rise to Fmax	Nuclear mutation	This report
stt7	+	R	WT	Defect in a thylakoid-associated protein kinase involved in LHCII phosphorylation	Depège et al. (2003)
AP6	−	HLS	ND	Mutation in nuclear gene PCY1	Kindle and Lawrence (1998)
ΔpsbD	−	HLS	ND	Deletion in chloroplast psbD gene	Minai et al. (2006)
ΔpsaB	−	HLS	ND	Deletion in chloroplast psaB gene	Redding et al. (1999)