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The transcriptional regulator MEIS2 sets up the ground state for palatal osteogenesis in mice

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F20%3A00539949" target="_blank" >RIV/68378041:_____/20:00539949 - isvavai.cz</a>

  • Result on the web

    <a href="https://www.jbc.org/article/S0021-9258(17)48561-9/fulltext" target="_blank" >https://www.jbc.org/article/S0021-9258(17)48561-9/fulltext</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1074/jbc.RA120.012684" target="_blank" >10.1074/jbc.RA120.012684</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    The transcriptional regulator MEIS2 sets up the ground state for palatal osteogenesis in mice

  • Original language description

    Haploinsufficiency of Meis homeobox 2 (MEIS2), encoding a transcriptional regulator, is associated with human cleft palate, and Meis2 inactivation leads to abnormal palate development in mice, implicating MEIS2 functions in palate development. However, its functional mechanisms remain unknown. Here we observed widespread MEIS2 expression in the developing palate in mice. Wnt1(Cre)-mediated Meis2 inactivation in cranial neural crest cells led to a secondary palate cleft. Importantly, about half of the Wnt1(Cre),Meis2(f/f) mice exhibited a submucous cleft, providing a model for studying palatal bone formation and patterning. Consistent with complete absence of palatal bones, the results from integrative analyses of MEIS2 by ChIP sequencing, RNA-Seq, and an assay for transposase-accessible chromatin sequencing identified key osteogenic genes regulated directly by MEIS2, indicating that it plays a fundamental role in palatal osteogenesis. De novo motif analysis uncovered that the MEIS2-bound regions are highly enriched in binding motifs for several key osteogenic transcription factors, particularly short stature homeobox 2 (SHOX2). Comparative ChIP sequencing analyses revealed genome-wide co-occupancy of MEIS2 and SHOX2 in addition to their colocalization in the developing palate and physical interaction, suggesting that SHOX2 and MEIS2 functionally interact. However, although SHOX2 was required for proper palatal bone formation and was a direct downstream target of MEIS2, Shox2 overexpression failed to rescue the palatal bone defects in a Meis2-mutant background. These results, together with the fact that Meis2 expression is associated with high osteogenic potential and required for chromatin accessibility of osteogenic genes, support a vital function of MEIS2 in setting up a ground state for palatal osteogenesis.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10605 - Developmental biology

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2020

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Journal of Biological Chemistry

  • ISSN

    0021-9258

  • e-ISSN

  • Volume of the periodical

    295

  • Issue of the periodical within the volume

    16

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    20

  • Pages from-to

    5449-5460

  • UT code for WoS article

    000530288000021

  • EID of the result in the Scopus database

    2-s2.0-85083575339