Serial thin section movie of every third section from the DTC to the distal extensions of Sh1 in a young adult hermaphrodite posterior gonad arm

Gap-junctional signaling mediates myriad cellular interactions in
metazoans. Yet, how gap junctions control the positioning of cells in
organs is not well understood. Innexins compose gap junctions in
invertebrates and affect organ architecture. Here, we investigate the
roles of gap-junctions in controlling distal somatic gonad architecture
and its relationship to underlying germline stem cells in Caenorhabditis
elegans. We show that a reduction of soma-germline gap-junctional activity
causes displacement of distal sheath cells (Sh1) towards the distal end of
the gonad. We confirm, by live imaging, transmission electron microscopy,
and antibody staining, that bare regions – lacking somatic gonadal cell
coverage of germ cells – are present between the distal tip cell
(DTC) and Sh1, and we show that an innexin fusion protein used in a prior
study encodes an antimorphic poisonous gap junction subunit that
mispositions Sh1. We determine that, contrary to the model put forth in
the prior study based on this fusion protein, Sh1 mispositioning does not
markedly alter the position of the borders of the stem cell pool nor of
the progenitor cell pool. Together, these results demonstrate that gap
junctions can control the position of Sh1, but that Sh1 position is
neither relevant for GLP-1/Notch signaling nor for the exit of germ cells
from the stem cell pool.