Xenbase Image ID: 158603

Fig. 7. Hypothetical model ofhmmr functionduring anterior neural tube closure. (A) Elongated cell with polarized microtubule (MT) cytoskeleton in control embryo. (B) During neural fold apposition, cells of the superficial (dark grey) and deep (light gray) layer interdigitate, pulling lateral cells towards the midline (Davidson and Keller, 1999). Upon neural tube closure, cells finalize radial intercalation (RI) to form a unilayered epithelium which re-establishes a ventricular lumen. Far lateral cell populations (green) are directed towards the midline to establish the roof plate (Davidson and Keller, 1999). During further brain development, the roof plate invaginates forming e.g. the septum, which separates the telencephalic hemispheres. (C) Loss of hmmr disturbs cell elongation and MT polarization. (D) During neural tube closure, RI and, consequently, narrowing of neural tissue fails. After neural tube closure, lateral cell populations remain separated which prevents formation of a functional roof plate. (E) Conspicuous morphological differences are apparent in neural tube closure between forebrain and hindbrain / spinal cord regions. PCP components in general are required along the entire anterior-posterior neural axis (white). PCP proteins mediate RI along the entire neural axis (dark blue), while their function in mediolateral intercalation and convergent extension (MLI / CE) is restricted to the hindbrain and spinal cord level (light blue). Together, the two PCP protein-driven processes MLI / CE and RI bring about posterior neural tube closure and spinal cord morphogenesis. Anterior neural tube closure and forebrain morphogenesis is facilitated by PCP protein-driven RI alone. Image published in: Prager A et al. (2017) Copyright © 2017. Image reproduced with permission of the Publisher, Elsevier B. V. Larger Image Printer Friendly View

Return to previous page