Oct 2026· Developmental Biology· Vol 541, pp. 109397· 0 citations· 28 references
Medicine
TL;DR
Data suggest that primary cilia require IFT70A for full function, and altered hedgehog signaling in the mutant hindlimb indicates the likely downstream mechanism by which IFT70A function contributes to digit patterning.
Abstract
The function of IFT70A has been explored with a combination of loss of function in vitro experiments and Xenopus depletions. These data suggest that primary cilia require IFT70A for full function. Here we employed a mouse model to investigate the consequences of an IFT70A deletion. Using CRISPR/Cas9 gene editing, we targeted the two mouse homologs Ift70a1 and Ift70a2 to generate deletion alleles of each individually (Ift70a1null; Ift70a2null), and an allele in which both genes are removed (Ift70a1/a2null). Ift70a1null/null and Ift70a1/a2null/null double knockout mice exhibited partially penetrant hindlimb polydactyly, but no other phenotype was observed. Altered hedgehog signaling in the mutant hindlimb indicates the likely downstream mechanism by which IFT70A function contributes to digit patterning.
The mouse genome encodes two
Lefty
genes that antagonize NODAL signaling to break symmetry during gastrulation. Despite their central regulatory role, accurately describing and comparing their embryonic function remains unclear. Here, we generated high replicate powered single-cell transcriptional atlases of
Lef...
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