In Arabidopsis, seeds within a single silique develop at a similar rate. If the homozygous insertion in AtINH3 causes embryo lethality, the self-pollinated seeds from heterozygous inh3 mutants would be expected to include aborted seeds. In wild-type siliques, all seeds developed normally and were green in color (Fig. 6D). However, the heterozygous lines of inh3-1 and inh3-2 produced 24.6% and 22.2% white or brown shriveled seeds, respectively (Table II  

Table II.

Percentages of aborted seeds in wild-type and inh3 mutants


Allele

Normal Seeds

Aborted Seeds

Total
Wild type96.5%3.5%n = 85
inh3-1 selfed75.4%24.6%n = 135
inh3-2 selfed
77.8%
22.2%
n = 99

Allele

Normal Seeds

Aborted Seeds

Total
Wild type96.5%3.5%n = 85
inh3-1 selfed75.4%24.6%n = 135
inh3-2 selfed
77.8%
22.2%
n = 99
Table II.

Percentages of aborted seeds in wild-type and inh3 mutants


Allele

Normal Seeds

Aborted Seeds

Total
Wild type96.5%3.5%n = 85
inh3-1 selfed75.4%24.6%n = 135
inh3-2 selfed
77.8%
22.2%
n = 99

Allele

Normal Seeds

Aborted Seeds

Total
Wild type96.5%3.5%n = 85
inh3-1 selfed75.4%24.6%n = 135
inh3-2 selfed
77.8%
22.2%
n = 99
), and the segregation ratio of normal to abnormal seeds was approximately 3:1, suggesting that these aborted seeds might have been the missing homozygous mutants. Furthermore, the mature dried seeds from wild-type plants exhibited a light brown color and were uniform in shape, whereas the seeds from heterozygous inh3 mutants contained a number of shriveled and dark brown seeds (Supplemental Fig. S3). Taken together, these results suggest that the disruption of AtINH3 causes embryo lethality in Arabidopsis. We thus focused our attention on the role of Inh3 in early embryogenesis.

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