We have been studying a locus that affects the assembly timing of the major chlorophyll protein complex, LHCII, an antenna complex for photosystem II. Previous work (MNL 60:44) has shown that inbred Mo17 carries an allele (Mof*-1) that allows premature assembly of LHCII in v24-576 (previously designated v*-576) material. A second allele, Mof*-2, segregated in the original material segregating v24 -576, and rendered LHCII assembly abnormally late. Heterozygous material, Mof*-1 Mof*-2, had apparently normal assembly timing of LHCII. The effect of Mof* on LHCII assembly is only observed in virescent material and not in normal siblings.
To test whether Mof*-2 is unmasked by other v24 alleles, the F2 progenies were examined for a cross between V24 V24 Mof*-1 Mof*-2 and V24 v24-424 Mof*-1 Mof*-1 (see accompanying figure for pedigree of parental genotypes and for information that substantiates genotype assignment; v244-24 was previously designated v*-424). The original material segregating v24-424 has shown no evidence of the Mof*-2 trait. Our backcrossing program for V24 alleles has until recently only involved Mo17 (Mof*-1 Mof*-1). Within each progeny segregating virescent seedlings, 16-25 v seedlings were tested for Mof*-1 or Mof*-2 by combined criteria of leaf chlorophyll induction kinetics and initial fluorescence yield (described in MNL 60:44). Confirmation of the LHCII assembly timing with fluorescence was obtained for two progenies by analyses of thylakoid polypeptides. The data show that Mof*-2 can also act on v24-424. Four of nine progenies segregated only v seedlings with early LHCII assembly (Mof*-1 Mof*-1) while the remaining five segregated u seedlings with early, normal and late LHCII assembly (Mof*-1 Mof*-2 selfed).
In progress: We are testing (1) whether Mof* is linked to any cab loci that encode apo-proteins of LHCII, (2) whether Mof* can affect timing of LHCII assembly of other u mutations (v, v3, v5, v12, v16), and (3) whether any inbred lines carry Mof*-2.
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