Germline soma communication mediated by gap junction proteins regulates epithelial morphogenesis

Abstract

Gap junction (GJ) proteins, the primary constituents of GJ channels, are conserved determinants of patterning. Canonically, a GJ channel, made up of two hemi-channels contributed by the neighboring cells, facilitates transport of metabolites/ions. Here we demonstrate the involvement of GJ proteins during cuboidal to squamous epithelial transition displayed by the anterior follicle cells (AFCs) from Drosophila ovaries. Somatically derived AFCs stretch and flatten when the adjacent germline cells start increasing in size. GJ proteins, Innexin2 (Inx2) and Innexin4 (Inx4), functioning in the AFCs and germline respectively, promote the shape transformation by modulating calcium levels in the AFCs. Our observations suggest that alterations in calcium flux potentiate STAT activity to influence actomyosin-based cytoskeleton, possibly resulting in disassembly of adherens junctions. Our data have uncovered sequential molecular events underlying the cuboidal to squamous shape transition and offer unique insight into how GJ proteins expressed in the neighboring cells contribute to morphogenetic processes.

Ecdysone Orchestrates Notch and Broad Symphony to Craft Epithelial Cell Shape Change

“…From the observation we can infer that acto-myosin contractility network is altered in Ecdysone depleted cells. This accumulation of zipper is quite similar with inx2 depleted cells (Sahu et al, 2021).…”

Mating-induced ecdysone in the testis disrupts soma-germline contacts and stem cell cytokinesis

“…1A) (Sarkar et al, 2007;Amy A. Kiger et al, 2000). Soma-germline contacts are then stabilized and maintained by adherens and septate junctions as they co-differentiate (Sahu et al, 2021;Fairchild et al, 2016). Using extended live imaging of the stem cell niche, we find that mating disrupts GSC cytokinesis by decreasing soma-germline contacts.…”

TOR signalling regulates epithelial cell shape transition inDrosophilaoogenesis

“…Previous studies have shown that the stage 8 cuboidal follicle cells undergo a conspicuous increase in cell size to acquire flattened squamous cell fate in the developing egg chambers 7,21,[25][26][27] . Consistent with the previous report, we also observed that the area of squamous cells is approximately 30 times (1316±87.1 SEM µm 2 ) than that of their cuboidal precursors (26.49±1.915 SEM µm 2 ) (Fig 1A).…”

“…Using FLIPOUT mediated system, we randomly generated mosaics of TOR RNAi overexpressing clusters in the follicle cells. The cuboidal-to-squamous-shape transition of AFCs is a two-step process involving the shrinkage of the lateral membrane (flattening) followed by stretching of the flattened cells to acquire the squamous fate 26 . The TOR RNAi clones were identified by GFP expression and unlike the control where the AFCs have completely stretched, TOR-depleted AFCs were smaller and exhibited a defect in stretching in the stage 10 egg chambers (Control: 768.3±38.01 SEM µm 2 ; TOR RNAi : 374.4±29.9 SEM µm 2 ) (Fig 1I -O).…”

“…Further it has been reported that the TGF beta signaling regulates the timing of this transition 7 . The transitioning of cuboidal to squamous fate is presumed to be a two-step process where the lateral membrane of the cuboidal cells shrinks followed by the stretching of flattened follicle cells 26 . The flattening of the cuboidal follicle cells is aided by the removal of lateral protein Fas2 by the Ser/Thr kinase Tao 27 .…”