AbstractAmongst the different accessions of Arabidopsis thaliana, a triploid block leading to seed abortion is frequent in crosses between diploid mothers and the pollen derived from Col -0 tetraploids. On the other hand, crosses involving diploid mothers and most other tetraploid pollen parents result in largely healthy seeds. This post-zygotic barrier is established in the endosperm, and the genetic basis underlying this phenomenon has been attributed to parental genomic imprinting. However, the molecular mechanisms explaining the survival
continuum of triploid F1 populations across Arabidopsis accessions are largely unclear. The research reported in this thesis has utilised the genetic variation in Arabidopsis to identify the genomic regions harbouring the maternal modifiers of the Col-killer effect in different accessions. Distinct chromosomal regions were identified in Bla-1, C24 and Tsu-0 accessions. While the Bla-1 and C24 maternal modifiers map to the TTG2 locus residing at the lower end
of chromosome 2, an additional locus on chromosome 4 was mapped in the C24 accession, suggesting that C24 recruits at least two loci to maternally repress the Col-killer to produce a high frequency of viable seeds. The Tsu-0 accession, on the other hand, recruits the TTG1 locus on the upper arm of chromosome 5 as a maternal modifier of the triploid block. The maternal TTG1 loss of function significantly improved the frequency of seed survival in Ler-0 and a mixed Ler-0 background, but at a substantially lower rate in the Col-0 genetic background; a strong indication that different accessions recruit distinct genes to repress
the Col-killer. Additionally, the concomitant decrease in proanthocyanidin accumulation in both TTG1 and TTG2 mutants was associated with maternal rescue. However, the effectiveness of TTG1/TTG2 mitigation is dependent on the genetic backgrounds involved and the level of killing of the tetraploid pollen used. Furthermore, the genetic analysis in this study shows that TTG1 functions synergistically with auxin to regulate seed size but does so independently of TTG2. This work provides insights into the maternal role of the TTG1-TTG2
complex in the flavonoid biosynthesis pathway as both genes may not be functionally equivalent in seed size control. Therefore, these findings established a genetic framework for understanding seed size regulation and the evolutionary forces shaping the genetic variation of triploid F1 seed survival in Arabidopsis.
|Date of Award||11 Oct 2021|
|Supervisor||James Doughty (Supervisor), Roderick Scott (Supervisor) & Baoxiu Qi (Supervisor)|