Seed dormancy is an adaptive trait whereby germination is blocked under favourable conditions to avoid germination out of season. Over time mature dry seeds lose dormancy and gradually acquire the capacity to germinate. Dormancy levels, i.e. the time required to release dormancy of the newly produced dry seed, are influenced by the environment of the mother plant and particularly by cold temperatures, which increase dormancy levels. It is also known that the seed coat, a maternal dead tissue, is important to keep seeds dormant over time, probably by shielding the seed living tissues from atmospheric oxygen.

Biochemical and genetical evidence previously established that cold promotes polyester accumulation in the seed coat and mutant seeds deficient in polyester biosynthesis have low dormancy and viability. However, it is unclear which seed coat structures, such as apoplastic barriers, are remodeled or created de novo in response to cold during seed development.

Combining histological and genetical approaches, I discovered a previously uncharacterized apoplastic barrier located in the outer integument 1 (oi1) cell layer. This barrier is strongly reinforced by cold and this process requires a MYB transcription factor (TF), specifically expressed in oi1 cells. I showed that mutants lacking the MYB TF, lacking the barrier, are less dormant, providing direct evidence that this barrier promotes dormancy in Arabidopsis thaliana. Thus, the temperature plasticity of this barrier acts as a memory in molecule storage form to control subsequently seed germination.