The molecular mechanisms underlying lethality of F1 hybrids between diverged parents are one target of speciation research. Crosses between diploid
and tetraploid individuals of the same genotype can result in F1 lethality, and this dosage-sensitive incompatibility plays a role in polyploid
speciation.
The authors have identified variation in F1 lethality in interploidy crosses of Arabidopsis thaliana and determined the genetic
architecture of the maternally expressed variation via QTL mapping. A single large-effect QTL, DR. STRANGELOVE 1 (DSL1), was identified as well as two
QTL with epistatic relationships to DSL1. DSL1 affects the rate of postzygotic lethality via expression in the maternal sporophyte. Fine mapping
placed DSL1 in an interval encoding the maternal effect transcription factor TTG2. Maternal parents carrying loss-of-function mutations in TTG2
suppressed the F1 lethality caused by paternal excess interploidy crosses.
The frequency of cellularization in the endosperm was similarly affected by
both natural variation and ttg2 loss-of-function mutants. The simple genetic basis of the natural variation and effects of single-gene mutations
suggests that F1 lethality in polyploids could evolve rapidly.
Furthermore, the role of the sporophytically active TTG2 gene in interploidy crosses
indicates that the developmental programming of the mother regulates the viability of interploidy hybrid offspring.
Citation
The maternally expressed WRKY transcription factor TTG2 controls
lethality in
interploidy crosses of Arabidopsis.
Dilkes BP, Spielman M, Weizbauer R, Watson B, Burkart-Waco D, et al. (2008)
PLoS Biol 6(12): e308. doi:10.1371/journal.pbio.0060308
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