FoxN3 is necessary for the development of the interatrial septum, the ventricular trabeculae and the muscles at the head/trunk interface in the African clawed frog, Xenopus laevis (Lissamphibia: Anura: Pipidae)

Abstract

Background Fox genes are a large family of transcription factors that play diverse roles in the immune system, metabolism, cancer, cell cycle, and animal development. It has been shown that FoxN3 is indispensable for normal craniofacial development in the mouse and the African clawed frog, Xenopus laevis. Morpholino‐mediated knockdown of FoxN3 in X. laevis delays overall development of early tadpole stages and causes eye defects, the absence of some cranial nerve branches, and malformations of the cranial skeleton and some cranial muscles, while the skeleton, nerves and muscles of the trunk are unaffected. Results We report a delay in heart morphogenesis, the absence of the interatrial septum, and a reduction and compaction of the ventricular trabeculation after knockdown of FoxN3 in X. laevis. Furthermore, we found malformations of the cucullaris and diaphragmatico‐branchialis muscles, two head muscles that develop in the head/trunk interface of X. laevis. Conclusions FoxN3 is necessary for the development of the interatrial septum and trabeculae in the frog heart, as well as the cranial muscles developing in the head/trunk interface. This gives the first evidence for a dependence on the head myogenic program of the cucullaris muscle in an anuran species.

Emergence of heart and branchiomeric muscles in cardiopharyngeal mesoderm

“…These signaling pathways may regulate cell fate choices within a pool of progenitor cells primed for heart and head muscle fates rather than acting on individual bipotent cells. Finally, work in Xenopus has shown that the transcription factor FoxN3 is required in the anuran branchiomeric neck muscle program as well as for development of the venous pole of the heart, although the underlying mechanisms remain to be resolved [87].…”

Acetylation of Checkpoint suppressor 1 enhances its stability and promotes the progression of triple-negative breast cancer

“…Chromatin Immunoprecipitation (ChIP)-seq and structural analysis found that CHES1 was a bispecific transcription factor which recognized a canonical forkhead (FKH) motif as well as alternate lower affinity (FHL) motif simultaneously [ 19 , 20 ]. Functionally, CHES1 modulated many cellular procedures, such as cell cycle arrest [ 15 , 21 ], embryogenesis [ 22 , 23 ], glucose metabolism [ 24 ], insulin sensitivity [ 25 ] and DNA damage response [ 16 ]. Moreover, the regulatory role of CHES1 has been established in various malignancies, and its dysfunction has been associated with outcome of patients [ 26 , 27 ].…”