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Hippo signaling instructs ectopic but not normal organ growth [Liver YapHyper]

ABSTRACT: Hippo signaling instructs ectopic but not normal organ growth [Liver YapHyper]

PROVIDER: PRJNA870448 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21103365.fastq.gz	Fastqsanger.gz
	SRR21103366.fastq.gz	Fastqsanger.gz
	SRR21103367.fastq.gz	Fastqsanger.gz
	SRR21103368.fastq.gz	Fastqsanger.gz
	SRR21103369.fastq.gz	Fastqsanger.gz

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Hippo signaling instructs ectopic but not normal organ growth

Project description:Hippo signaling instructs ectopic but not normal organ growth

| PRJNA870441 | ENA

Hippo signaling instructs ectopic but not normal organ growth [Drosophila YkiHyper]

Project description:Hippo signaling instructs ectopic but not normal organ growth [Drosophila YkiHyper]

| PRJNA870447 | ENA

Hippo signaling instructs ectopic but not normal organ growth [Drosophila NonPupatingLarvae]

Project description:Hippo signaling instructs ectopic but not normal organ growth [Drosophila NonPupatingLarvae]

| PRJNA870446 | ENA

Hippo signaling instructs ectopic but not normal organ growth [Liver YapTazKO+CCl4]

Project description:Hippo signaling instructs ectopic but not normal organ growth [Liver YapTazKO+CCl4]

| PRJNA870449 | ENA

Hippo signaling instructs ectopic but not normal organ growth [Drosophila YkiHyper]

Project description:In order to study how ectopic Yki drives tissue overgrowth in Drosophila imaginal discs, we overexpressed the constitutively active Yki3SA and deleted wts in clones of cells in the entire eye-antennal imaginal disc, as well as specifically in eye disc proper cells using Optix-Gal4. Using the MARCM system allowed us to compare the effects of Yki3SA overexpression in wild-type and sd mutant clones.

2022-11-19 | GSE211458 | GEO

Hippo signaling instructs ectopic but not normal organ growth

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-18 | GSE211461 | GEO

Hippo signaling instructs ectopic but not normal organ growth [Drosophila NonPupatingLarvae]

Project description:We fed wildtype larvae a special diet that lacks precursor molecules necessary for the synthesis of the molting hormone ecdysone required for pupation, thus keeping animals in the larval stage. Importantly, in these larvae, the imaginal discs grow until their terminal size is reached but they do not proceed with differentiation as this requires a pulse of ecdysone. This method thus allowed us to directly compare actively growing discs with discs at the same developmental stage that terminated proliferation after reaching their proper size.

2022-11-19 | GSE211457 | GEO

Hippo signaling instructs ectopic but not normal organ growth [Liver YapHyper]

Project description:We conditionally activated Yap in hepatocytes of adult mice by two different methods: we deleted the Lats1/2 kinases via injecting AAV8-Cre into Lats1/2 double floxed mice (Lats1/2 KO) and we overexpressed YAP via doxycycline feeding of mice that expressed the tetracycline-activated transactivator (rtTA) under the hepatocyte-specific ApoE promoter and human YAP from a rtTA-responsive TetO promoter (Apo>YAP).

2022-11-19 | GSE211459 | GEO

Hippo signaling instructs ectopic but not normal organ growth [Liver YapTazKO+CCl4]

Project description:We conditionally deleted Yap/Taz from hepatocytes prior to induction of acute injury by injection of liver toxin carbon tetrachloride (CCl4).

2022-11-19 | GSE211460 | GEO

Organ growth control in the absence of Hippo signaling

Project description:Organs of all animals reliably grow to a specific size and it is widely thought that such developmental growth control is instructed by the Hippo signaling pathway. This is based on studies in flies and mice showing that deregulation of Hippo signaling causes dramatic tissue overgrowth of various organs. Here we use two major developmental paradigms and provide evidence that removing the key transcriptional downstream effectors of the Hippo pathway does not abolish organ growth control. Specifically, eliminating the function of the Hippo downstream co-activators Yki as well as Yap/Taz that complex with TEAD family transcription factors did not interfere with organ growth control in the developing mouse liver or Drosophila eye. Rather, mutant cells were able to proliferate appropriately during development, properly exit the cell cycle, and form organs of normal size. Remarkably, a complementing whole transcriptome analysis of mutant Drosophila eye imaginal discs corroborated these genetic findings. It showed that loss of the single TEAD transcription factor Scalloped (Sd) fully reverted the effect of overexpression of hyperactivated Yki back to a wildtype gene expression profile. In contrast, Sd/Yap/Taz proved to be crucial for cell survival in injury response models, namely X-ray irradiation of flies and toxic liver injury in mice. Therefore, we propose that Hippo signaling is dispensable for instructing normal organ growth and instead suggest that the classical Hippo mutant overgrowth phenotypes represent a de facto Yap/Taz/Yki gain-of-function situation that does not reflect an endogenous role in growth control. Instead, we hypothesize that the potency of Yap/Taz/Yki to drive tissue overgrowth draws from their broad and primary function in injury responses.

2025-02-28 | GSE96887 | GEO

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