PgmNr W4038: A Potential Role for Midbodies in Developing Tissues of C. elegans.

Authors:
J. N. Bembenek 1 ; X. Bai 1 ; B. C. Chen 2 ; R. Simmons 1 ; C. Turpin 1 ; L. Uehlein 1 ; D. Mitchell 1 ; E. Betzig 2


Institutes
1) University of Tennessee, Knoxville, Knoxville, TN; 2) Janelia Research Campus, HHMI, Ashburn, VA.


Keyword: Cytokinesis

Abstract:

The midbody forms at the end of cytokinesis and facilitates abscission, the final separation of the daughter cells. Midbodies have been implicated in several cellular processes in addition to abscission including cell fate, dorsoventral axis formation, neurite growth, and apical polarity during epithelial lumen formation. To investigate midbody function we examined midbody fate in the invariant lineage of the C. elegans embryo.  Live-cell imaging has revealed unique and tissue-specific patterns of the fate of the midbody and different midbody components.  In early embryo cell divisions, midbody flank proteins are lost from the midbody soon after cytokinesis while proteins associated with the midbody ring persists for much longer. A dramatic shift in midbody behavior is observed in several tissues at around the 300-cell stage when the embryo undergoes global morphogenetic changes. In two lumen-forming tissues, the gut and pharynx, midbodies form and migrate to the apical midline. This midbody migration event coincides with previously characterized polarization events in gut epethelia. Upon reaching the intestinal midline the midbody ring is internalized and disappears; however, the Aurora B kinase, AIR-2, remains on the apical surface for over an hour after polarization. A similar apical localization pattern is observed for AIR-2 in the pharyngeal primordium. AIR-2 also localizes to midbodies in the sensilla primordium, which aggregate in foci over multiple successive divisions. AIR-2 persists along the leading edge of developing dendrites as they migrate towards the anterior end of the embryo and extend as dendritic processes. Other midbody markers are either internalized and degraded or maintained with AIR-2 in a tissue-specific manner. Inactivation of the central spindle organizer, spd-1, disrupted Aurora B kinase localization to the midbody as expected. However, Aurora B kinase was still capable of accumulating on the apical surface possibly by localizing to centrosomes. Inactivating several fast-inactivating temperature sensitive cytokinesis mutants late in embryogenesis causes severe morphogenesis defects. We hypothesize that the midbody and specific cytokinesis regulators such as AIR-2 may regulate the final interphase architecture of a terminally dividing cell.



Wormbase Genetic Index
1. air-2
2. spd-1