In vivo RNAi screen identifies candidate signaling genes required for collective cell migration in Drosophila ovary

Luo, Jun; Zuo, JunTao; Wu, Jing; Wan, Ping; Kang, Di; Cao, Xiang; Zhu, Hong; Chen, Jiong

doi:10.1007/s11427-014-4786-z

Cited by 18 publications

(19 citation statements)

References 73 publications

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“…Second, Src42A promotes the detachment of the cluster from the follicular epithelium and third, the limitation of the Src42A protein and activity is required in order to maintain the morphology and integrity of the cluster during collective cell migration. While previous studies have shown that constitutive activation of Src42A impedes border cell migration (Luo et al, 2015;Somogyi and Rørth, 2004), we show the requirement for, and the pattern of activity of, Src42A during this process.…”

Section: Discussioncontrasting

confidence: 55%

“…Over-expression of Src WT results in a large increase and ectopic localization of active Src in border cells, suggesting that negative regulators are limiting. One such negative regulator appears to be the receptor for activated C kinase, Rack (Luo et al, 2015), though its mechanism of activation and action remain to be determined.…”

Section: Regulation Of Src Expression Levels and Activity Are Essentialmentioning

confidence: 99%

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Src42A required for collective border cell migrationin vivo

Sallak

Torres

Yin³

et al. 2017

Preprint

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The tyrosine kinase Src is over-expressed in numerous human cancers and is associated with poor prognosis. While Src has been extensively studied, its contributions to collective cell migration in vivo remain incompletely understood. Here we show that Src42A, but not Src64, is required for the specification and migration of the border cells in the Drosophila ovary, a well-developed and genetically tractable in vivo cell migration model. We found active Src42A enriched at border cell/nurse cell interfaces, where E-cadherin is less abundant, and depleted from border cell/border cell and border cell/polar cell junctions where E-cadherin is more stable, whereas total Src42A protein co-localizes with E-cadherin. Over-expression of wild type Src42A mislocalized Src activity and prevented border cell migration. Constitutively active or kinase dead forms of Src42A also impeded border cells. These findings establish border cells as a model for investigating the mechanisms of action of Src in cooperative, collective, cell-on-cell migration in vivo.

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Section: Discussioncontrasting

confidence: 55%

Section: Regulation Of Src Expression Levels and Activity Are Essentialmentioning

confidence: 99%

Src42A required for collective border cell migrationin vivo

Sallak

Torres

Yin³

et al. 2017

Preprint

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“…This phenotype is statistically significant, yet less severe than other RNAi phenotypes for other genes [e.g. brk ; (Luo et al, 2015)]. These results suggest that neo plays a general, previously uncharacterized role in supporting migration in two distinct cell types; further characterization of the similarities and differences between the mechanisms involving neo in CVM and BCs would be an interesting avenue for future study.…”

Section: Resultsmentioning

confidence: 71%

Comparative analysis of gene expression profiles for several migrating cell types identifies cell migration regulators

Bae

Macabenta

Curtis

et al. 2017

Mechanisms of Development

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Cell migration is an instrumental process that ensures cells are properly positioned to support the specification of distinct tissue types during development. To provide insight, we used fluorescence activated cell sorting (FACS) to isolate two migrating cell types from the Drosophila embryo: caudal visceral mesoderm (CVM) cells, precursors of longitudinal muscles of the gut, and hemocytes (HCs), the Drosophila equivalent of blood cells. ~350 genes were identified from each of the sorted samples using RNA-seq, and in situ hybridization was used to confirm expression within each cell type or, alternatively, within other interacting, co-sorted cell types. To start, the two gene expression profiling datasets were compared to identify cell migration regulators that are potentially generally-acting. 73 genes were present in both CVM cell and HC gene expression profiles, including the transcription factor Zinc finger homeodomain-1 (Zfh1). Comparisons with gene expression profiles of Drosophila border cells that migrate during oogenesis had a more limited overlap, with only the genes neyo (neo) and singed (sn) found to be expressed in border cells as well as CVM cells and HCs, respectively. neo encodes a protein with Zona pellucida domain linked to cell polarity, while sn encodes an actin binding protein. Tissue specific RNAi expression coupled with live in vivo imaging was used to confirm cell-autonomous roles for Zfh1 and Neo in supporting CVM cell migration, whereas previous studies had demonstrated a role for Sn in supporting HC migration. In addition, comparisons were made to migrating cells from vertebrates. Seven genes were found expressed by chick neural crest cells, CVM cells, and HCs including extracellular matrix (ECM) proteins and proteases. In summary, we show that genes shared in common between CVM cells, HCs, and other migrating cell types can help identify regulators of cell migration. Our analyses show that Neo in addition to Zfh1 and Sn studied previously impact cell migration. This study also suggests that modification of the extracellular milieu may be a fundamental requirement for cells that undergo cell streaming migratory behaviors.

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“…Previous studies suggest the monomeric FBS consensus sequence is PyCAAGGPyCPu or PyGAAGGPyCPu (36). Three possible FBSs were predicted in the 3-kb promoter region of Mmp2: GGAAGGTCA (Ϫ2604 to Ϫ2595), AGGCCTTGA (Ϫ2326 to Ϫ2317), and TCAAGGCTG (Ϫ1254 to Ϫ1263) (Fig.…”

Section: Hormonal Control Of Mmp-induced Fat Body Cell Dissociation Imentioning

confidence: 90%

Juvenile hormone and 20-hydroxyecdysone coordinately control the developmental timing of matrix metalloproteinase–induced fat body cell dissociation

Jia

Liu

Wen

et al. 2017

Journal of Biological Chemistry

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Tissue remodeling is a crucial process in animal development and disease progression. Coordinately controlled by the two main insect hormones, juvenile hormone (JH) and 20-hydroxyecdysone (20E), tissues are remodeled context-specifically during insect metamorphosis. We previously discovered that two matrix metalloproteinases (Mmps) cooperatively induce fat body cell dissociation in However, the molecular events involved in this Mmp-mediated dissociation are unclear. Here we report that JH and 20E coordinately and precisely control the developmental timing of Mmp-induced fat body cell dissociation. We found that during the larval-prepupal transition, the anti-metamorphic factor Kr-h1 transduces JH signaling, which directly inhibited expression and activated expression of tissue inhibitor of metalloproteinases () and thereby suppressed Mmp-induced fat body cell dissociation. We also noted that upon a decline in the JH titer, a prepupal peak of 20E suppresses Mmp-induced fat body cell dissociation through the 20E primary-response genes, and, which inhibited expression of the nuclear receptor and competence factor β Moreover, upon a decline in the 20E titer, β expression was induced by the 20E early-late response gene , and then βftz-F1 directly activated expression and inhibited expression, causing Mmp-induced fat body cell dissociation during 6-12 h after puparium formation. In conclusion, coordinated signaling via JH and 20E finely tunes the developmental timing of Mmp-induced fat body cell dissociation. Our findings shed critical light on hormonal regulation of insect metamorphosis.

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In vivo RNAi screen identifies candidate signaling genes required for collective cell migration in Drosophila ovary

Cited by 18 publications

References 73 publications

Src42A required for collective border cell migrationin vivo

Src42A required for collective border cell migrationin vivo

Comparative analysis of gene expression profiles for several migrating cell types identifies cell migration regulators

Juvenile hormone and 20-hydroxyecdysone coordinately control the developmental timing of matrix metalloproteinase–induced fat body cell dissociation

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