spalt is functionally conserved in Locusta and Drosophila to promote wing growth

Wang, Dan; Li, Juanjuan; Liu, Suning; Zhou, Hang; Zhang, Long; Shi, Wangpeng; Shen, Jie

doi:10.1038/srep44393

Cited by 10 publications

(7 citation statements)

References 44 publications

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“…One was grouped cells extruding into the posterior region, which had connections to the major dpp expression region ( Fig. 1B-D, yellow arrowheads) and may be either proliferated (Wang et al, 2017) or migrated from the main part. The other was single cells, which were separated from the dpp expression region (Fig.…”

Section: Sal/sall4 Hyperactivation Stimulates Cell Invasionmentioning

confidence: 99%

“…Cell death pathways and the JNK signaling are activated in sal knockdown cells, but these two processes only have a minor role in generating the sal mutant phenotypes (Organista and De Celis, 2013;Organista et al, 2015). Conversely, ectopic sal expression promotes cell proliferation (Skottheim Honn et al, 2016;Wang et al, 2017) via positive regulation of the microRNA bantam (Wang et al, 2017). These results suggest that sal is vital in organ size control by accelerating cell proliferation, but the relation of Drosophila sal to tumorigenesis is not yet known.…”

Section: Introductionmentioning

confidence: 98%

“…In the wing disc, the expression of sal is activated by Decapentaplegic (Dpp) signaling in specific regions and leads to tissue growth (de Celis et al, 1996; Barrio and de Celis, 2004;Doumpas et al, 2013;Akiyama and Gibson, 2015). Loss of sal shows abnormal vein formation and reduction in wing size (de Celis et al, 1996;Grieder et al, 2009;Wang et al, 2017). At the cellular level, mitotic cells are strongly reduced in sal mutant wing discs (Organista and De Celis, 2013).…”

Section: Introductionmentioning

confidence: 99%

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The transcription factor spalt and human homologue SALL4 induce cell invasion via the dMyc-JNK pathway in Drosophila

et al. 2020

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Cancer cell metastasis is a leading cause of mortality in cancer patients. Therefore, revealing the molecular mechanism of cancer cell invasion is of great significance for the treatment of cancer. In human patients, the hyperactivity of transcription factor Spalt-like 4 (SALL4) is sufficient to induce malignant tumorigenesis and metastasis. Here, we found that when ectopically expressing the Drosophila homologue spalt (sal) or human SALL4 in Drosophila, epithelial cells delaminated basally with penetration of the basal lamina and degradation of the extracellular matrix, which are essential properties of cell invasion. Further assay found that sal/SALL4 promoted cell invasion via dMyc-JNK signaling. Inhibition of the c-Jun N-terminal kinase (JNK) signaling pathway through suppressing matrix metalloprotease 1, or basket can achieve suppression of cell invasion. Moreover, expression of dMyc, a suppressor of JNK signaling, dramatically blocked cell invasion induced by sal/SALL4 in the wing disc. These findings reveal a conserved role of sal/SALL4 in invasive cell movement and link the crucial mediator of tumor invasion, the JNK pathway, to SALL4-mediated cancer progression. This article has an associated First Person interview with the first author of the paper.

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Section: Sal/sall4 Hyperactivation Stimulates Cell Invasionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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The transcription factor spalt and human homologue SALL4 induce cell invasion via the dMyc-JNK pathway in Drosophila

et al. 2020

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“…Insects also appear to have two epipods dorsal to the insect coxa, because when “wing” genes are depleted in insects via RNAi, two distinct outgrowths are affected, the wing and the plate adjacent to the leg (Fig. 1c, ( 32 - 35 )).…”

Section: Main Textmentioning

confidence: 99%

Insect wings and body wall evolved from ancient leg segments

Bruce

Patel

2018

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“…The mechanisms underlying venation patterning in other insect lineages have remained poorly understood, and so far, gene expression patterns and functions for the few genes examined seem to be similar to those in Drosophila ( 16 – 18 ).…”

Section: Introductionmentioning

confidence: 99%

Molecular mechanism underlying venation patterning in butterflies

Banerjee

Monteiro

2020

Preprint

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The paper describes new domains of venation patterning genes in butterflies and proposes how 14 simplified venation in other insect lineages might have evolved. 15 16 Abstract 17 The mechanism of wing vein differentiation in Drosophila is a classic text-book example of 18 pattern formation using a system of positional-information, yet very little is known about how this 19 mechanism differs in species with a different number of veins and how insect venation patterns 20 evolved. Here, we examine the expression patterns of genes previously implicated in vein 21 differentiation in Drosophila in two butterfly species with more complex venation, the African 22 squinting bush brown Bicyclus anynana and the Asian cabbage white, Pieris canidia. We also test 23 the function of one of these genes, spalt (sal), with CRISPR-Cas9 in B. anynana. We identify 24 both conserved as well as new domains of decapentaplegic (dpp), engrailed (en), invected (inv) 25 and sal gene expression in B. anynana, and propose how the simplified venation in Drosophila 26 might have evolved via loss of dpp and sal gene expression domains, silencing of vein inducing 27 programs at Sal-expression boundaries, and changes in gene expression of vein maintenance 28 genes. 29 30 MAIN TEXT 31 32 45 47 vinegar fly Drosophila melanogaster, where a classic system of positional information takes 48 place. Here, the wing is initially sub-divided into two domains of gene expression, and anterior 49 and posterior compartment, where engrailed (en) and invected (inv) expression are restricted to 50 the posterior compartment (7, 8). A central linear morphogen source of the protein 51 Decapentaplegic (Dpp) is established at the posterior border of the anterior compartment, and 52 genes like spalt (sal) respond to the continuous morphogen gradient in a threshold-like manner, 53 creating sharp boundaries of gene expression that provide precise positioning for the longitudinal 54 veins (9, 10). Veins differentiate along these boundaries, along a parallel axis to the Dpp 55 morphogen source (11, 12). Vein cell identity is later determined by the expression of genes such 56 as rhomboid (rho), downstream of sal (10, 13). Conversely, intervein cells will later express 57 blistered (bls) which suppresses vein development (14, 15). The final vein positions are 58 determined by the cross-regulatory interaction of rho and bls. 59 60The mechanisms underlying venation patterning in other insect lineages have remained poorly 61 understood, and so far, gene expression patterns and functions for the few genes examined seem 62 to be similar to those in Drosophila (16-18). 64Venation patterning in butterflies (order: Lepidoptera) has been examined in a few mutants in 65 connection with alterations of color pattern development (19, 20) and more directly via the 66 expression pattern of a few genes during larval development. Two of the species in which a few 67 of the venation patterning genes have been studied in some detail are the African squinting bush 68 brown butterfly,...

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spalt is functionally conserved in Locusta and Drosophila to promote wing growth

Cited by 10 publications

References 44 publications

The transcription factor spalt and human homologue SALL4 induce cell invasion via the dMyc-JNK pathway in Drosophila

The transcription factor spalt and human homologue SALL4 induce cell invasion via the dMyc-JNK pathway in Drosophila

Insect wings and body wall evolved from ancient leg segments

Molecular mechanism underlying venation patterning in butterflies

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