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Sox10-cre BAC transgenes reveal temporal restriction of mesenchymal cranial
neural crest and identify glandular Sox10 expression.
Deal KK, Rosebrock JC, Eeds AM, DeKeyser JL, Musser MA, Ireland SJ, May-Zhang
AA, Buehler DP, Southard-Smith EM
Submitted Externally on 2/22/2021
Volume : Pages
471 : 119 - 137
Diversity of neural crest derivatives has been studied with a variety of
approaches during embryonic development. In mammals Cre-LoxP lineage tracing is
a robust means to fate map neural crest relying on cre driven from regulatory
elements of early neural crest genes. Sox10 is an essential transcription factor
for normal neural crest development. A variety of efforts have been made to
label neural crest derivatives using partial Sox10 regulatory elements to drive
cre expression. To date published Sox10-cre lines have focused primarily on
lineage tracing in specific tissues or during early fetal development. We
describe two new Sox10-cre BAC transgenes, constitutive (cre) and inducible
(cre/ERT2), that contain the complete repertoire of Sox10 regulatory elements.
We present a thorough expression profile of each, identifying a few novel sites
of Sox10 expression not captured by other neural crest cre drivers. Comparative
mapping of expression patterns between the Sox10-cre and Sox10-cre/ERT2
transgenes identified a narrow temporal window in which Sox10 expression is
present in mesenchymal derivatives prior to becoming restricted to neural
elements during embryogenesis. In more caudal structures, such as the intestine
and lower urinary tract, our Sox10-cre BAC transgene appears to be more
efficient in labeling neural crest-derived cell types than Wnt1-cre. The
analysis reveals consistent expression of Sox10 in non-neural crest derived
glandular epithelium, including salivary, mammary, and urethral glands of adult
mice. These Sox10-cre and Sox10-cre/ERT2 transgenic lines are verified tools
that will enable refined temporal and cell-type specific lineage analysis of
neural crest derivatives as well as glandular tissues that rely on Sox10 for
proper development and function.
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Financial support for this work was provided by the NIDDK Mouse Metabolic Phenotyping Centers (National MMPC, RRID:SCR_008997,
) under the MICROMouse Program, grants DK076169.
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