Exprimé durant les stades précoces du développement, XACT a la propriété de recouvrir les chromosomes X actifs (Xa). Mon laboratoire de thèse a identifié XACT, un lARNnc retrouvé uniquement chez les grands primates. Ces observations suggèrent l'existence d'un mécanisme chez l'humain qui bloquerait de manière transitoire l'action de XIST et contrôlerait la mise en place de l'XCI. Curieusement, à ce stade du développement, malgré la présence de XIST, ces chromosomes sont toujours activement transcrits. En effet, lors du développement préimplantatoire humain, XIST s'accumule sur les chromosomes X, chez la femelle et le mâle, observation que l'on ne retrouve pas dans le modèle murin. Principalement étudiée dans le modèle murin, un nombre croissant de preuves indiquent que l'ICX n'est pas mise en place de la même manière chez l'humain, même si la finalité reste la même. L'acteur principal de ce processus est XIST, un lARNnc, qui a la capacité de recouvrir et d'inactiver le chromosome à partir duquel il est exprimé. Ce processus est essentiel pour égaliser le dosage des produits des gènes liés à l'X, entre les mammifères mâles et femelles. L'inactivation du chromosome X (ICX) est un paradigme de régulation épigénétique impliquant des lARNnc. Nos connaissances sur ces lARNnc proviennent de l'étude d'une infime fraction de ces molécules, révélant leur implication dans de nombreux processus cellulaires, notamment la régulation de l'expression génique. L'évolution des études transcriptomiques a révélé une transcription pervasive chez les eucaryotes, produisant de nombreux ARN non codants, et notamment des longs ARNs non codants (lARNnc). Since the combination of XO and trisomy 16 does not severely affect early mouse development, it is likely that regulatory mechanisms essential for early embryogenesis do not function correctly in XnX16 embryos due to activity of the extra X chromosome segment of X16. Developmental abnormalities found in XnX16 embryos include: (1) growth retardation detected as early as stage 9, (2) continual loss of embryonic ectoderm cells either by death or by expulsion into the proamniotic cavity, (3) underdevelopment of the ectoplacental cone throughout the course of development, (4) very limited, if any, mesoderm formation, (5) failure in early organogenesis including the embryo, amnion, chorion and yolk sac. Since X chromosome inactivation does not occur in these embryos, probably due to the lack of the inactivation center on X16, XnX16 embryos are functionally disomic for the proximal 63% of the X chromosome and trisomic for the distal segment of chromosome 16. Matings between female mice carrying Searle's translocation, T(X 16)16H, and normal males give rise to chromosomally unbalanced zygotes with two complete sets of autosomes, one normal X chromosome and one X16 translocation chromosome (XnX16 embryos).
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