Alexandre Djiane's research while affiliated with Université de Montpellier and other places

... Our data suggests that hyperplasia without proliferation in the AG engages common tumorigenic gene networks described in other tumor models, even in the absence of mitosis (Hamaratoglu and Atkins, 2020; Khan et al., 2013;Logeay et al., 2022). In particular, we observed significant overlap with a common signature from the Drosophila metastatic tumor model of oncogenic Ras combined with the loss of epithelial polarity through loss of the Scribble protein (Ras V12 ,scrib-/-mutant) (Fig. 4C), (Atkins et al., 2016;Kulshammer et al., 2015) and wound healing gene expression profiles (Khan et al., 2017), Table 1). ...

... Primary antibodies used are listed below. Secondary Alexa Fluor Antibodies (1/600; Invitrogen) were used as described previously [20] for 1 h at room temperature before mounting the coverslips with Vectashield (Vector Laboratories #H-1200) and imaging on Zeiss Apotome or Leica Thunder microscopes. Antibodies used were rabbit anti-53BP1 (1/100; CST #4937), mouse anti-phospho-Histone H2AX clone JBW301 (1/200; Millipore #05-636), anti-TAZ (1/100; CST #4883), mouse anti-TEAD4 (1/50; Santa Cruz #sc101184), and rabbit anti-YAP (1/100; CST #14074). ...

... Knockdown of α-spectrin revealed it one of the candidate genes that resulted in a larger adult wing size. Spectrin proteins function with multiple interacting partners, including microtubules and actin filaments (Deng et al., 2020;Fletcher et al., 2015;Forest et al., 2018;Khanal et al., 2016). When α-spectrin was conditionally knocked down in wing epithelia using the nub-Gal4 driver (Forest et al., 2018), an increase in wing tissue size was observed (Fig. 1A, B). ...

... They yield a multi-protein complex interacting through a-catenin to actin filaments in the cell. A clustering of cadherin-catenin complexes on the cell membrane leads to local remodeling of intracellular actin and microtubules and facilitates the formation of cell-cell adherens junctions [39][40][41]. ...

... It is therefore tempting to speculate that PAR-3 and the ZO proteins act together to form phase-separated condensates that organize tight junctions and link them to the cytoskeleton. Many of the same proteins interact with Bazooka/ Par-3, including the nectin, ZO-1 and afadin orthologues (Echinoid, Pyd and Canoe), the sole fly MAGI protein and the RASSF8-ASPP2 complex, suggesting that a similar phase-separated condensate scaffolds the apical adherens junction in flies [79][80][81] . These condensates may be anchored to the plasma membrane through an interaction between a conserved C-terminal motif in Bazooka/Par-3 and the phosphoinositides (PI(4,5)P 2 and PI(3,4,5)P 3 ) 82-85 . ...

... 42,70,119 The Hippo signalling pathway is also modulated by extensive crosstalk with other signalling pathways. [42][43][44][45] These include signalling through G protein-coupled receptors (GPCRs), activated by either lipids (lysophosphatidic acid and sphingosine-1-phosphophate) or hormones (glucagon or adrenaline) 120-123 ; the WNT pathway, which can regulate YAP/TAZ either through incorporation into the β-catenin destruction complex or through destruction complexindependent mechanisms [124][125][126][127][128][129] ; SRC family kinases that promote YAP/TAZ nuclear localization and transcriptional activity either directly by phosphorylating tyrosine residues or indirectly by repressing LATS1/LATS2 13,62,[129][130][131][132][133][134] ; TGFβ signalling, which regulates YAP nuclear translocation by targeting the Hippo pathways scaffold RASSF1 135 ; the PI3K pathway, which either modulates the core Hippo cascade via PI3K-PDK1 or YAP/TAZ localization via AKTmediated phosphorylation 13,102,[136][137][138] ; the NOTCH pathway, which modulates YAP/TAZ levels and activity [139][140][141] This appears to be consistent with the reduced nuclear localization of YAP (and TAZ) in the basal epidermal cell layer of adult compared to foetal and neonatal mice. 13,123,144 However, conditional knockout of Yap/Taz in adult epidermis significantly impaired epidermal tissue repair upon skin wounding, 13 similar to topical treatment of skin wounds with YAP-interfering RNAs. ...

... In the wing disc, CycE is a downstream target gene of Notch to control proliferation. 67,68 Consistently, we found that CycE overexpression failed to rescue the loss of type II NBs caused by Notch knockdown (Figures 6C and 6D). It seems plausible that CycE serves as an independent regulatory role in cell proliferation rather than selfrenewal. ...

... One mechanical solution for robustly maintaining the tube diameter while allowing flexibility in tube curvature is to introduce periodic circumferential actin cables. Such structures are generally found in multiple systems at different length scales ranging from the nanometer to the micrometer scale, including neuronal processes 1 , vertebrate blood vessels 2 , the hypoderm of Caenorhabditis elegans embryos 3 , and Drosophila trachea 4 . Plant vessels are surrounded by circumferential cortical microtubules 5 . ...

... The recovered alleles were characterized by PCR amplification of the relevant genomic regions followed by sequencing analysis. Other alleles and stocks used in this work are: wild-type Oregon R; scramb1 MI01181 − GFSTF.0 (BDSC #60,164); dor 8 (BDSC, #28); Df(3R)pyd ex147 [69]; duf sps1 [10]; Past1 110.1 [48]; Amph 26 [70] and Flo2 KG00210 [42]. ...

... Finally, the interaction between PLXND1 and GIPCs might directly influence cell morphology via modulation of cytoskeletal dynamics. Support for this notion comes from genetic experiments in Drosophila and mammalian proteomic studies that implicate GIPCs and MYO6 in actin network stabilization (Djiane and Mlodzik, 2010;O'Loughlin et al., 2018;Isaji et al., 2011;Noguchi et al., 2006). ...