Neural transcription factors bias cleavage stage blastomeres to give rise to neural ectoderm.
The decision by embryonic ectoderm to give rise to epidermal versus neural derivatives is the result of signaling events during blastula and gastrula stages. However, there also is evidence in Xenopus that cleavage stage blastomeres contain maternally derived molecules that bias them toward a neural fate. We used a blastomere explant culture assay to test whether maternally deposited transcription factors bias 16-cell blastomere precursors of epidermal or neural ectoderm to express early zygotic neural genes in the absence of gastrulation interactions or exogenously supplied signaling factors. We found that Foxd4l1, Zic2, Gmnn, and Sox11 each induced explants made from ventral, epidermis-producing blastomeres to express early neural genes, and that at least some of the Foxd4l1 and Zic2 activities are required at cleavage stages. Similarly, providing extra Foxd4l1 or Zic2 to explants made from dorsal, neural plate-producing blastomeres significantly increased the expression of early neural genes, whereas knocking down either significantly reduced them. These results show that maternally delivered transcription factors bias cleavage stage blastomeres to a neural fate. We demonstrate that mouse and human homologs of Foxd4l1 have similar functional domains compared to the frog protein, as well as conserved transcriptional activities when expressed in Xenopus embryos and blastomere explants. genesis 54:334-349, 2016. © 2016 Wiley Periodicals, Inc.
Department of Anatomy and Regenerative Biology, School of Medicine and Health Sciences, George Washington University, Washington, DC.
Shailly
S
Gaur
Department of Anatomy and Regenerative Biology, School of Medicine and Health Sciences, George Washington University, Washington, DC.
Max
M
Mandelbaum
Department of Anatomy and Regenerative Biology, School of Medicine and Health Sciences, George Washington University, Washington, DC.
Mona
M
Herold
Department of Anatomy and Regenerative Biology, School of Medicine and Health Sciences, George Washington University, Washington, DC.
Himani Datta
HD
Majumdar
Department of Anatomy and Regenerative Biology, School of Medicine and Health Sciences, George Washington University, Washington, DC.
Karen M
KM
Neilson
George Washington University Institute for Neuroscience.
Thomas M
TM
Maynard
Laboratory of Cell and Developmental Signaling, National Cancer Institute, National Institutes of Health, Frederick, Maryland.
Kathy
K
Mood
Laboratory of Cell and Developmental Signaling, National Cancer Institute, National Institutes of Health, Frederick, Maryland.
Ira O
IO
Daar
Department of Anatomy and Regenerative Biology, School of Medicine and Health Sciences, George Washington University, Washington, DC.|George Washington University Institute for Neuroscience.
Sally A
SA
Moody
D000818:Animals; D001757:Blastomeres / Q000378:metabolism; D036703:Blastula / Q000254:growth & development; D002454:Cell Differentiation / Q000235:genetics*; D004475:Ectoderm / Q000254:growth & development* / Q000378:metabolism; D051858:Forkhead Transcription Factors / Q000096:biosynthesis / Q000235:genetics*; D005775:Gastrula / Q000254:growth & development; D018507:Gene Expression Regulation, Developmental; D006801:Humans; D051379:Mice; D054258:Neural Plate / Q000254:growth & development* / Q000378:metabolism; D014157:Transcription Factors / Q000096:biosynthesis / Q000235:genetics; D029867:Xenopus Proteins / Q000096:biosynthesis / Q000235:genetics; D014982:Xenopus laevis / Q000235:genetics / Q000254:growth & development; D015053:Zygote / Q000254:growth & development
D051858:Forkhead Transcription Factors; D014157:Transcription Factors; D029867:Xenopus Proteins; C491811:Zic2 protein, mouse
Foxd4; Foxd4l1; Foxd4l1.1; Foxd5; Sox11; Sox2; Zic1; Zic2; geminin; neural induction