Most important agricultural crop plants show shallow seed dormancy because this has been selected for during the domestication process. In some crops, including cereals, very low dormancy levels can lead to pre-harvest sprouting and consequently reduced product quality. The plant hormone abscisic acid is required for the induction of dormancy, whereas germination needs gibberellins. Mutants that affect bioactive levels, or interfere with the signalling pathways of these hormones, usually show seed dormancy phenotypes. Several other hormones also influence dormancy and germination usually by interaction with ABA. Ethylene for instance acts antagonistically to ABA and promotes endosperm rupture. Recently, a role for 12-oxophytodienoic acid in germination repression has been identified that is synergistic with ABA. Despite the knowledge at the hormone level, the control of seed dormancy at the molecular level is still poorly understood. When free peptides meet a bacteria, they will first be captured and bound to the target cell, and then the cellular membrane would be divided into two different parts, namely the peptide-free and the peptide-bound leaflets, in which the lipids are either free of or associated with the peptides. Mechanically, the elastic modulus of the peptide-bound leaflets would be larger than that of the peptide-free leaflets, because the bound peptides on the membrane were like crusted patches, which would not only limit the undulation of the bound lipids but also weaken the elastic deformability of the peptide-bound leaflets. It illustrates that there would have a step variance of the elastic modulus over the edge of a crusted patch for the bound membrane. Through accumulation of the bound peptides, the elastic modulus of the membrane would not only increase, just as the case of the red cell bound with ligands, but also become more and more non-uniform. Thus, under active or passive movement of the cellular membrane, the transient or prolonged stress concentration would occur at the edges between peptide-free and peptide-bound leaflets, and then facilitate the formation of some slots or pores in the membrane. Obviously, a more rigid bound peptide would imply a stronger constraint to the longitudinal and transversal fluctuations of the bound lipids in a peptide-bound leaflet, leading a more significant stress concentration to occur at the edge of the peptide-bound leaflet, and further making the peptide-bound leaflet be torn more easily away from the cellular membrane. It may provide a mechanical explanation for the observation that, prior to pore formation.