Salvador-Warts-Hippo Pathway in a Developmental Checkpoint Monitoring Helix-Loop-Helix Proteins

Wang, Lan Hsin; Baker, Nicholas E.

doi:10.1016/j.devcel.2014.12.002

Cited by 27 publications

(42 citation statements)

References 116 publications

(151 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent work illustrates that dysregulated HLH transcription factors are sufficient to activate the Hippo signalling pathway. Results from this work demonstrate that the hyperactive Hippo pathway indeed contributes to apoptosis dependent upon the elimination of Yki/YAP/TAZ activity [94]. So far, connections between HLH proteins and core components of the Hippo pathway have not been proposed as direct causes of particular diseases or defects.…”

Section: Resultsmentioning

confidence: 99%

“…The Hippo pathway has been shown to be regulated by the important transcriptional regulators of organogenesis, E proteins and ID proteins [94,95]. The widely expressed E proteins belong to the basic helix-loop-helix (bHLH) family, which heterodimerize with tissue-specific bHLH proteins to regulate cell growth, commitment and differentiation in many tissues [96,97].…”

Section: Hyperactivation Of the Hippo Pathwaymentioning

confidence: 99%

See 1 more Smart Citation

Disease implication of hyper-Hippo signalling

Wang

2016

Open Biol.

Self Cite

View full text Add to dashboard Cite

The Hippo signalling pathway regulates cellular proliferation, apoptosis and differentiation, thus exerting profound effects on cellular homeostasis. Inhibition of Hippo signalling has been frequently implicated in human cancers, indicating a well-known tumour suppressor function of the Hippo pathway. However, it is less certain whether and how hyperactivation of the Hippo pathway affects biological outcome in living cells. This review describes current knowledge of the regulatory mechanisms of the Hippo pathway, mainly focusing on hyperactivation of the Hippo signalling nexus. The disease implications of hyperactivated Hippo signalling have also been discussed, including arrhythmogenic cardiomyopathy, Sveinsson's chorioretinal atrophy, Alzheimer's disease, amyotrophic lateral sclerosis and diabetes. By highlighting the significance of disease-relevant Hippo signalling activation, this review can offer exciting prospects to address the onset and potential reversal of Hippo-related disorders.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Hyperactivation Of the Hippo Pathwaymentioning

confidence: 99%

Disease implication of hyper-Hippo signalling

Wang

2016

Open Biol.

Self Cite

View full text Add to dashboard Cite

show abstract

“…Emc is the Drosophila Inhibitor of DNA binding (Id) protein homolog and a negative regulator of bHLH-mediated differentiation (Campuzano, 2001). Emc contributes to cell proliferation in the wing disc and undifferentiated eye disc by restricting the activity and expression of the bHLH protein Daughterless (Bhattacharya and Baker, 2011; Wang and Baker, 2015). Another potential target could be myc , which is an important target of mammalian Notch during leukemogenesis (Weng et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

The Notch pathway regulates the Second Mitotic Wave cell cycle independently of bHLH proteins

Bhattacharya

Quiquand

et al. 2017

Developmental Biology

View full text Add to dashboard Cite

Notch regulates both neurogenesis and cell cycle activity to coordinate precursor cell generation in the differentiating Drosophila eye. Mosaic analysis with mitotic clones mutant for Notch components was used to identify the pathway of Notch signaling that regulates the cell cycle in the Second Mitotic Wave. Although S phase entry depends on Notch signaling and on the transcription factor Su(H), the transcriptional co-activator Mam and the bHLH repressor genes of the E(spl)-Complex were not essential, although these are Su(H) coactivators and targets during the regulation of neurogenesis. The Second Mitotic Wave showed little dependence on ubiquitin ligases neuralized or mindbomb, and although the ligand Delta is required non-autonomously, partial cell cycle activity occurred in the absence of known Notch ligands. We found that myc was not essential for the Second Mitotic Wave. The Second Mitotic Wave did not require the HLH protein Extra macrochaetae, and the bHLH protein Daughterless was required only cell-nonautonomously. Similar cell cycle phenotypes for Daughterless and Atonal were consistent with requirement for neuronal differentiation to stimulate Delta expression, affecting Notch activity in the Second Mitotic Wave indirectly. Therefore Notch signaling acts to regulate the Second Mitotic Wave without activating bHLH gene targets.

show abstract

“…Transcriptional reporters for hid and rpr were elevated in all Rp/+ cells, most of which were not apoptotic ( Figure 1). As Rp/+ cells do not transcribe higher levels of DIAP1, 56 elevated rpr or hid may sensitize Rp/+ cells to cell death without being the specific trigger. Elevating DIAP1 after rpr, grim and hid deletion might de-sensitize Rp/+ cells, rather than block a specific pathway.…”

Section: /P53mentioning

confidence: 99%

Apoptotic mechanisms during competition of ribosomal protein mutant cells: roles of the initiator caspases Dronc and Dream/Strica

Kale

Lee

et al. 2015

Cell Death Differ

View full text Add to dashboard Cite

Heterozygosity for mutations in ribosomal protein genes frequently leads to a dominant phenotype of retarded growth and small adult bristles in Drosophila (the Minute phenotype). Cells with Minute genotypes are subject to cell competition, characterized by their selective apoptosis and removal in mosaic tissues that contain wild-type cells. Competitive apoptosis was found to depend on the pro-apoptotic reaper, grim and head involution defective genes but was independent of p53. Rp/+ cells are protected by anti-apoptotic baculovirus p35 expression but lacked the usual hallmarks of 'undead' cells. They lacked Dronc activity, and neither expression of dominant-negative Dronc nor dronc knockdown by dsRNA prevented competitive apoptosis, which also continued in dronc null mutant cells or in the absence of the initiator caspases dredd and dream/strica. Only simultaneous knockdown of dronc and dream/strica by dsRNA was sufficient to protect Rp/+ cells from competition. By contrast, Rp/Rp cells were also protected by baculovirus p35, but Rp/Rp death was dronc-dependent, and undead Rp/Rp cells exhibited typical dronc-dependent expression of Wingless. Independence of p53 and unusual dependence on Dream/Strica distinguish competitive cell death from noncompetitive apoptosis of Rp/Rp cells and from many other examples of cell death.

show abstract

Salvador-Warts-Hippo Pathway in a Developmental Checkpoint Monitoring Helix-Loop-Helix Proteins

Cited by 27 publications

References 116 publications

Disease implication of hyper-Hippo signalling

Disease implication of hyper-Hippo signalling

The Notch pathway regulates the Second Mitotic Wave cell cycle independently of bHLH proteins

Apoptotic mechanisms during competition of ribosomal protein mutant cells: roles of the initiator caspases Dronc and Dream/Strica

Contact Info

Product

Resources

About