RESUMEN
Introduction: Mutations in the FOXE1 gene are implicated in cleft palate and thyroid dysgenesis in humans. Methods: To investigate whether zebrafish could provide meaningful insights into the etiology of developmental defects in humans related to FOXE1, we generated a zebrafish mutant that has a disruption in the nuclear localization signal in the foxe1 gene, thereby restraining nuclear access of the transcription factor. We characterized skeletal development and thyroidogenesis in these mutants, focusing on embryonic and larval stages. Results: Mutant larvae showed aberrant skeletal phenotypes in the ceratohyal cartilage and had reduced whole body levels of Ca, Mg and P, indicating a critical role for foxe1 in early skeletal development. Markers of bone and cartilage (precursor) cells were differentially expressed in mutants in post-migratory cranial neural crest cells in the pharyngeal arch at 1 dpf, at induction of chondrogenesis at 3 dpf and at the start of endochondral bone formation at 6 dpf. Foxe1 protein was detected in differentiated thyroid follicles, suggesting a role for the transcription factor in thyroidogenesis, but thyroid follicle morphology or differentiation were unaffected in mutants. Discussion: Taken together, our findings highlight the conserved role of Foxe1 in skeletal development and thyroidogenesis, and show differential signaling of osteogenic and chondrogenic genes related to foxe1 mutation.
RESUMEN
Conjugated polymers with narrow band gaps are particularly useful for sorting and discriminating semiconducting single-walled carbon nanotubes (s-SWCNT) due to the low charge carrier injection barrier for transport. In this paper, we report two newly synthesized narrow-band-gap conjugated polymers (PNDITEG-TVT and PNDIC8TEG-TVT) based on naphthalene diimide (NDI) and thienylennevinylene (TVT) building blocks, decorated with different polar side chains that can be used for dispersing and discriminating s-SWCNT. Compared with the mid-band-gap conjugated polymer PNDITEG-AH, which is composed of naphthalene diimide (NDI) and head-to-head bithiophene building blocks, the addition of a vinylene linker eliminates the steric congestion present in head-to-head bithiophene, which promotes backbone planarity, extending the π-conjugation length and narrowing the band gap. Cyclic voltammetry (CV) and density functional theory (DFT) calculations suggest that inserting a vinylene group in a head-to-head bithiophene efficiently lifts the highest occupied molecular orbital (HOMO) level (-5.60 eV for PNDITEG-AH, -5.02 eV for PNDITEG-TVT, and -5.09 eV for PNDIC8TEG-TVT). All three polymers are able to select for s-SWCNT, as evidenced by the sharp transitions in the absorption spectra. Field-effect transistors (FETs) fabricated with the polymer:SWCNT inks display p-dominant properties, with higher hole mobilities when using the NDI-TVT polymers as compared with PNDITEG-AH (0.6 cm2 V-1 s-1 for HiPCO:PNDITEG-AH, 1.5 cm2 V-1 s-1 for HiPCO:PNDITEG-TVT, and 2.3 cm2 V-1 s-1 for HiPCO:PNDIC8TEG-TVT). This improvement is due to the better alignment of the HOMO level of PNDITEG-TVT and PNDIC8TEG-TVT with that of the dominant SWCNT specie.
RESUMEN
Constriction of the cytokinetic ring, a circular structure of actin filaments, is an essential step during cell division. Mechanical forces driving the constriction are attributed to myosin motor proteins, which slide actin filaments along each other. However, in multiple organisms, ring constriction has been reported to be myosin independent. How actin rings constrict in the absence of motor activity remains unclear. Here, we demonstrate that anillin, a non-motor actin crosslinker, indispensable during cytokinesis, autonomously propels the contractility of actin bundles. Anillin generates contractile forces of tens of pico-Newtons to maximise the lengths of overlaps between bundled actin filaments. The contractility is enhanced by actin disassembly. When multiple actin filaments are arranged into a ring, this contractility leads to ring constriction. Our results indicate that passive actin crosslinkers can substitute for the activity of molecular motors to generate contractile forces in a variety of actin networks, including the cytokinetic ring.
