The studies of the viviparous mutants of corn have yielded some information as to the loci of the genes involved.
Indications are that the mutants vp1 and vp4 obtained from Cornell are allelic. Linkage studies give no indications of this gene being located on the short arm of chromosome nine or the long arm of chromosorme ten. These are the loci for vp4 and vp1 respectively, reported in the literature. Crosses of stocks of this mutant with translocations B‑9a, B‑9b and B‑10 have revealed that the gene is not within the regions included in these translocations. Crosses with C, R, wx and sh give no indication of linkage with any of these genes. Apparent linkage with aleurone color, previously reported for this mutant, seems to be the result of the inhibition of color development when the gene is present in the homozygous condition.
A backcross of vp2 has yielded 29.5% crossing over between vp2 and pr, which is in good agreement with values previously reported.
Previous crosses of vp5 with translocation B‑1b had indicated that this mutant was in the short arm of chromosome one. A backcross of an F1 heterozygous for vp5 and translocation 1‑9a indicate 29.9% croosing over between the mutant and the translocation.
A three point test of vp7, pr and gl8 indicates the follawing order and map distances: vp7 14.6 pr 1.0 gl8. This data is in agreement with the order of these genes indicated by Dr. Sprague.
Viviparous had previously been located in the long arm of chromosome one with the aid of translocation B‑1a. Backcrosses of F1 plants heterozygous for this mutant: br, bm2 and translocation 1‑7c indicate the following order and map distances: (br) T 32.5 vp8 13.2 bm2. No crossovers were obtained between br and the translocation out of of 103 plants observed.
F2 data from plants heterozygous for vp9 and translocation 7‑9a‑76 indicate that this mutant is on chromosome seven. Crosses with translocation B-7b give no evidence of the gene being included in the translocated portion of chromosome seven, thus the gene is probably proximal to the break in this chromosome.
Physiological studies of normal and viviparous embryos seem to indicate that the combimtion of low oxygen tension and high CO2 tension is responsible for preventing germination of normal embryos during the development of the caryopsis. Concentrations of approximately 1% O2, 30% CO2 and 69% N2 will greatly retard the elongation of the plumule of excised normal embryos of immature seed without inhibiting the enlargement of the scutellum which will elongate from .5 to 1.5 mm in six days under these conditions. The plumules of vp5 embryos, obtained from the same selfed ear as the normals mentioned above, are not inhibited by these gas concentrations. This would suggest that embryos of this mutant germinate prematurely because they are capable of plumule elongation under conditions of low and high CO2, which possibly exist within the pericarp of developing seeds.
D. S. Robertson