Isolation of a mutable hcf*-19 allele

Two nuclear loci have been identified that block photosystem II (PSII) assembly: hcf3 (chromosome arm 1S) and hcf19 (tentatively assigned to chromosome 3L; it is uncovered by a confirmed TB-3La stock but linkage to known markers remains to be established). The molecular basis of the mutant phenotype is unknown. A second phenotype is associated with mutation at the hcf19 locus: low PSII activity with no apparent block in the insertion of PSII-polypeptides into thylakoids.

A line which had only segregated hcf individuals with the second hcf19 phenotype described above (based on electrophoretic analysis of thylakoid polypeptides for separate individuals) generated some progenies that segregated hcf seedlings with the same hcf19 phenotype as the parental material and others with green and yellow green sectors (see Table 1). The leaf chlorophyll fluorescence induction kinetics for yellow green sectors indicated a PSII lesion. While I have tentatively called the mutation mutable hcf19, allelism tests need to be made to confirm this assignment. The F2 progenies of crosses to mutable wx testers for Spm and Ac were generated in the summer of 1984 and are being analyzed.

Table 1. Segregation of hcf19 and mutable hcf19 in three F3 progenies of a cross between +/hcfl9 and inbred Mo17. This material is 12.5% EMS-treated genome, the remainder being 12.5% N28, 50% Mo17 and 12.5% some other line.
Total hcf (no sectors) hcf-m  Percent hcf + hcf-m
72 3 13 22.2
24 5 1 25.0
17 0 29.4

In any given progeny segregating mutable hcf19, sectors were both large and small, and in some instances were clonal. The yellow green sectors were not noticeable on first expansion of leaves and became apparent as plants matured. These sectored plants could be grown to maturity in the field, all producing pollen and some producing a small ear.

The segregation of mutable and non-mutable hcf19 in some progenies suggests a two element system is involved. If true, the suitability of using this particular mutable allele to clone hcf19 is dubious. Defective mobile elements have a good chance of being homologous to multiple regions on the genome, as has been established for Ds. However, identification of the inserted element would indicate that the locus is susceptible to insertion of a particular transposon class. This knowledge would be useful for future direction to this site of a transposon amenable to cloning the hcf19 locus.

M. Polacco

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