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Background  Little is known about the involvement of molecular determinants of segmental patterning of rhombomeres (r) in the development of rhythmic neural networks in the mouse hindbrain. Here, we compare the phenotypes of mice carrying targeted inactivations of  Hoxa2 , the only  Hox  gene expressed up to r2, and of  Krox20 , expressed in r3 and r5. We investigated the impact of such mutations on the neural circuits controlling jaw opening and breathing in newborn mice, compatible with Hoxa2-dependent trigeminal defects and direct regulation of  Hoxa2  by Krox20 in r3.    Results  We found that  Hoxa2  mutants displayed an impaired oro-buccal reflex, similarly to  Krox20  mutants. In contrast, while  Krox20  is required for the development of the rhythm-promoting parafacial respiratory group (pFRG) modulating respiratory frequency,  Hoxa2  inactivation did not affect neonatal breathing frequency. Instead, we found that  Hoxa2  -/-  but not  Krox20  -/-  mutation leads to the elimination of a transient control of the inspiratory amplitude normally occurring during the first hours following birth. Tracing of r2-specific progenies of  Hoxa2  expressing cells indicated that the control of inspiratory activity resides in rostral pontine areas and required an intact r2-derived territory.    Conclusion  Thus, inspiratory shaping and respiratory frequency are under the control of distinct  Hox -dependent segmental cues in the mammalian brain. Moreover, these data point to the importance of rhombomere-specific genetic control in the development of modular neural networks in the mammalian hindbrain.

Distinct roles of Hoxa2 and Krox20in the development of rhythmic neural networks controlling inspiratory depth, respiratory frequency, and jaw opening