Abstract
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. We 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.
Highlights
Postzygotic lethality of the hybrid offspring from crosses between divergent parents functions as a barrier that drives or reinforces speciation [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16]
Many flowering plants tolerate changes in the number of genome copies, but offspring of parents with different ploidies often fail to develop. We investigated this phenomenon in Arabidopsis thaliana and discovered variation in the ability to survive interploidy matings
TESTA GLABRA2 (TTG2) regulates the fate of interploidy crosses, and knock-outs of TTG2 improved the outcome of interploidy matings in both Ler and Col
Summary
Postzygotic lethality of the hybrid offspring from crosses between divergent parents functions as a barrier that drives or reinforces speciation [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16]. An example of F1 lethality occurs when progeny from crosses between newly formed polyploid individuals and their diploid progenitors fail during seed development. This lethality arises in the absence of any allelic diversity due to the difference in the dosage of genomes provided by the parents. The strength of this reproductive isolation can vary within species and between individuals of the same species, and has long been known to contribute to speciation. We understand neither the genetic basis of this barrier nor the source of variation within and between species
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
