Daughterless dictates Twist activity in a context-dependent manner during somatic myogenesis

Wong, Ming-Ching; Castanon, Irinka; Baylies, Mary K.

doi:10.1016/j.ydbio.2008.02.020

Cited by 20 publications

(38 citation statements)

References 55 publications

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“…These functions are independent of the dimer type and appear to be tissue-dependent in Drosophila. This switchable behavior is linked to a particular conserved domain of Da, which inactivates both Twi and Da transactivation domains through an intramolecular mechanism (Wong et al, 2008). As the domain is conserved across species, we anticipate that it similarly dictates TWIST tissue-specific effects in higher organisms.…”

Section: Twist Proteins Are Pleiotropic Gene Regulatorsmentioning

confidence: 97%

TWISTing an embryonic transcription factor into an oncoprotein

et al. 2010

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Over the past decade, the reactivation of TWIST embryonic transcription factors has been described as a frequent event and a marker of poor prognosis in an impressive array of human cancers. Growing evidence now supports the premise that these cancers hijack TWIST's embryonic functions, granting oncogenic and metastatic properties. In this review, we report on the history and recent breakthroughs in understanding TWIST protein functions and the emerging role of the associated epithelialmesenchymal transition (EMT) in tumorigenesis. We then broaden the discussion to address the general contribution of reactivating embryonic programs in cancerogenesis.

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Section: Twist Proteins Are Pleiotropic Gene Regulatorsmentioning

confidence: 97%

TWISTing an embryonic transcription factor into an oncoprotein

et al. 2010

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“…The following reporters were used: m6-GFP (Lai et al, 2000); 4.0Him-GFP (Rebeiz et al, 2002); aos NRE -lacZ, aos NREmutSu(H) -lacZ, edl NRE -lacZ (Krejci et al, 2009);and m8-lacZ (Kramatschek and Campos-Ortega, 1994). In overexpression and RNAi experiments, Gal4 driver stocks [1151:Gal4 (Anant et al, 1998), Ptc:Gal4 Tub:Gal80 ts , sca:Gal4] were combined with UAS lines [UAS:twi (Baylies and Bate, 1996), UAS-Ni 79.2 ] and/or RNAi lines [UAS-Notch-RNAi (BL7078), UAS-twi-RNAi (GD37092), UAS-da-RNAi (GD51297) (Dietzl et al, 2007), UAS-twiRNAi2x (Wong et al, 2008)] and larvae were shifted to 30°C 48 hours before dissections. Immunofluorescence was performed as described previously (Cooper and Bray, 1999) 1:500; gift of F. Martin and G. Morata (Herranz et al, 2008)], rabbit anti-Roughest [1/50; gift of K. Fishbach (Schneider et al, 1995)].…”

Section: Drosophila Experimentsmentioning

confidence: 99%

Specificity of Notch pathway activation: Twist controls the transcriptional output in adult muscle progenitors

et al. 2010

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SUMMARYCell-cell signalling mediated by Notch regulates many different developmental and physiological processes and is involved in a variety of human diseases. Activation of Notch impinges directly on gene expression through the Suppressor of Hairless [Su(H)] DNA-binding protein. A major question that remains to be elucidated is how the same Notch signalling pathway can result in different transcriptional responses depending on the cellular context and environment. Here, we have investigated the factors required to confer this specific response in Drosophila adult myogenic progenitor-related cells. Our analysis identifies Twist (Twi) as a crucial co-operating factor. Enhancers from several direct Notch targets require a combination of Twi and Notch activities for expression in vivo; neither alone is sufficient. Twi is bound at target enhancers prior to Notch activation and enhances Su(H) binding to these regulatory regions. To determine the breadth of the combinatorial regulation we mapped Twi occupancy genome-wide in DmD8 myogenic progenitor-related cells by chromatin immunoprecipitation. Comparing the sites bound by Su(H) and by Twi in these cells revealed a strong association, identifying a large spectrum of co-regulated genes. We conclude that Twi is an essential Notch co-regulator in myogenic progenitor cells and has the potential to confer specificity on Notch signalling at over 170 genes, showing that a single factor can have a profound effect on the output of the pathway.

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“…The LTs are thin, elongated fibers with dorsal/ventral orientations. Seven iTFencoding genes are expressed in the LT muscles, including Krüppel (Kr) , apterous (ap) (Bourgouin et al 1992), muscle segment homeobox (msh) (Nose et al 1998), araucan (ara)/caupolican (caup) (CarrascoRando et al 2011), twist (twi) (Wong et al 2008), and lateral muscles scarcer (lms) (Muller et al 2010). Though similar in shape, the four LT muscles can be distinguished from each other by positional information and gene expression patterns.…”

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confidence: 99%

Muscle Cell Fate Choice Requires the T-Box Transcription Factor Midline in Drosophila

et al. 2015

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Drosophila Midline (Mid) is an ortholog of vertebrate Tbx20, which plays roles in the developing heart, migrating cranial motor neurons, and endothelial cells. Mid functions in cell-fate specification and differentiation of tissues that include the ectoderm, cardioblasts, neuroblasts, and egg chambers; however, a role in the somatic musculature has not been described. We identified mid in genetic and molecular screens for factors contributing to somatic muscle morphogenesis. Mid is expressed in founder cells (FCs) for several muscle fibers, and functions cooperatively with the T-box protein H15 in lateral oblique muscle 1 and the segment border muscle. Mid is particularly important for the specification and development of the lateral transverse (LT) muscles LT3 and LT4, which arise by asymmetric division of a single muscle progenitor. Mid is expressed in this progenitor and its two sibling FCs, but is maintained only in the LT4 FC. Both muscles were frequently missing in mid mutant embryos, and LT4-associated expression of the transcription factor Krüppel (Kr) was lost. When present, LT4 adopted an LT3-like morphology. Coordinately, mid misexpression caused LT3 to adopt an LT4-like morphology and was associated with ectopic Kr expression. From these data, we concluded that mid functions first in the progenitor to direct development of LT3 and LT4, and later in the FCs to influence whichever of these differentiation profiles is selected. Mid is the first T-box factor shown to influence LT3 and LT4 muscle identity and, along with the T-box protein Optomotor-blind-related-gene 1 (Org-1), is representative of a new class of transcription factors in muscle specification. KEYWORDS midline; Tbx20; founder cell; muscle identity; differentiation T HE body wall muscles of the Drosophila larva are composed of a stereotypic pattern that includes 30 unique muscle fibers (each a single myotube) per abdominal hemisegment (Bate 1990). These muscles form during embryogenesis, during which time they take on unique characteristics such as size, shape, pattern of innervation, and epidermal attachment Baylies et al. 1998;Frasch 1999;De Joussineau et al. 2012). The unique identity of each muscle fiber is conferred through overlapping signaling pathways and cell autonomous transcription factors that specify muscle progenitors Baylies et al. 1998;Frasch 1999;Tixier et al. 2010), which then undergo asymmetric cell division to generate founder cells (FCs) (Bate 1990;Carmena et al. 1998). A single FC initiates the formation of multinucleate syncytia by fusing with fusion competent myoblasts (FCMs) (Rochlin et al. 2010;Abmayr and Pavlath 2012). FCs dictate the number of cell fusion events that take place, leading to a characteristic number of nuclei for each muscle in the pattern . These fusing nuclei adopt the transcriptional profile of the original FC nucleus (Bourgouin et al. 1992;D'Alessio and Frasch 1996;Ruiz-Gomez et al. 1997;Jagla et al. 1998;Keller et al. 1998;Nose et al. 1998;Crozatier and Vincent 1999;Knirr et al. 1999;D...

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Daughterless dictates Twist activity in a context-dependent manner during somatic myogenesis

Cited by 20 publications

References 55 publications

TWISTing an embryonic transcription factor into an oncoprotein

TWISTing an embryonic transcription factor into an oncoprotein

Specificity of Notch pathway activation: Twist controls the transcriptional output in adult muscle progenitors

Muscle Cell Fate Choice Requires the T-Box Transcription Factor Midline in Drosophila

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