Highlights in DD


  • Julie Kiefer

“Highlights” calls attention to exciting advances in developmental biology that have recently been reported in Developmental Dynamics. Development is a broad field encompassing many important areas. To reflect this fact, the section will spotlight significant discoveries that occur across the entire spectrum of developmental events and problems: from new experimental approaches, to novel interpretations of results, to noteworthy findings utilizing different developmental organisms.

The Genetics of Bad Teeth (Dev Dyn236:2980–2992) Know anyone with discolored, misshapen, and abnormally sized teeth? It could be that genetics, and not poor hygiene, are to blame. Gonadotropin-releasing hormone-1 (GnRH-1) and its receptor are expressed in incisor papillary layer cells and secretory amelioblasts, cell types involved in production and biomineralization of tooth enamel. Consistent with a role in this process, incisors in GnRH-1 mutant mice are larger and discolored (whiter) compared with wild-type, phenotypes that signal changes in secretion, deposition, or mineral transport during biomineralization. Furthermore, elemental analysis of iron, phosphorous, and calcium in mutant incisors shows a mass increase of each, and micro-CT analysis shows an increase in bone mineral density. Mutant incisors display no overt changes in cell proliferation or cell death, indicating GnRH-1 likely functions in attenuating enamel formation.

Banking on β-catenin (Dev Dyn236:3007–3019) β-Catenin's work never ends. First, it induces dorsal–ventral axis formation, and later it regulates specification of dorsal mesoderm derivatives. Domingo and colleagues reveal nuanced roles for β-catenin that could expose a relationship between these early and later events. In Xenopus where maternal β-catenin is morpholino-depleted, embryos arrest at gastrulation due to aberrant morphogenetic processes: blastomere cleavage planes are irregular, bottle cells form erratically, cells involute into the blastopore haphazardly, and convergent extension fails. Surprisingly, cells from morphant embryos are still competent to form dorsal mesodermal cell types, notochord and muscle. Clumps of morphant cells can differentiate into these cell types when grafted into a wild-type host. However, wild-type cells transplanted into a morphant host fail to differentiate. These experiments show that β-catenin is required to non–cell-autonomously maintain dorsal mesoderm. The authors argue that this event is dependent upon tissue interactions that take place during wild-type gastrulation movements.

A Kafkaesque Metamorphosis (Dev Dyn236:3173–3179) Kafka himself could not have dreamed up a more macabre scenario. Drosophila that bear hypomorphicTBP-related factor 2 (dTrf2) alleles make it only partway through life-cycle changes, their corpses a disturbing combination of their pre- and postmetamorphic selves. Work by Bashirullah et al. reveals the molecular underpinnings of the phenotypes. TRFs are a component of core transcription machinery that can replace TBP, making distinct TFIIDs that bind specific sets of promoters. The alleles characterized above are deficient in a dTRF2 transcript isoform that is most abundantly expressed in larval and pupal stages, accounting for their arrest during these times. Mutant phenotypes, incomplete head eversion, blocks in midgut and salivary gland cell death, and a misshapen puparium among them, suggest defects in ecdysone-mediated metamorphic events. In agreement, mutants show delayed expression and reduced abundance in ecdysone-response genes. Importantly, dTrf2 expression is not downstream of ecdysone, supporting the idea that the TRF directly regulates transcription of ecdysone-responsive genes. With molecular characterization of stage-specific dTrf2 functions to come, the next chapter of this story promises to be equally gripping.