Fig 4. Dynamics of Hox interactions indicates different roles for auto-regulation, posterior induction and posterior prevalence in A-P patterning.

(A) Q-PCR for HoxD1 at st.10.5, 11, 12 and 15 in WT and HoxB4 GR (activated at st.8) injected embryos. (B) Q-PCR for HoxB4 at st.10.5 and 11 in WT and HoxB4 injected embryos. (C) Q-PCR for HoxB6 at st.11 and 11.5 in WT and HoxB4 injected embryos. (D) Q-PCR for HoxB9 at st.11.5 and 12 in WT and HoxB4 injected embryos. (E) The known facts concerning auto-regulation, posterior induction and posterior prevalence in A-P Patterning. (a) Hox genes start to be expressed from early gastrulation onward in the non-organiser mesoderm (NOM), where there are high levels of BMP. At this stage, their nested expression domains overlap fully with each other. (b) During gastrulation and early neurulation, auto-regulation (A) and posterior induction (PI) together enable Hox genes (coloured discs) to be expressed in a temporal order that matches their 3' to 5' order on the chromosome (temporal collinearity) The sequential times of initial expression of the neighbouring Hox genes are indicated by the small clock faces. Since the precise control of Hox activation time is vital to function, posterior induction (black arrows) may possibly occur in a cascade manner to ensure the expression of Hox genes in the correct order. Data is not presently available to determine whether this is the case. Starting from neurulation, posterior prevalence (PP) exerts its influence in neurectoderm and paraxial mesoderm, where there are relatively low levels of BMP. The coordination between auto-regulation, posterior induction and posterior prevalence during this stage helps to establish a pre-pattern, resulting in non-overlapping or partially overlapping expression. Notably, posterior prevalence does not happen in a cascade manner since it is not required for driving the Hox timer. Later during axis elongation, these earlier events lead to a spatial pattern being established (spatial collinearity).