Table 1.

Documented Yki/YAP/TAZ interactions with chromatin-modifying proteins.

Interacting Chromatin Modifying Protein or Complex	Conclusion	Reference(s)
SWI/SNF complex (direct)	Brahma–Yki/Sd interact in the nucleus.	[29,30,32]
	Brahma–Yki/Sd bind to Yki targets.	[30,32]
	Knockdown of Brahma inhibits Yki-mediated tissue overgrowth.	[32]
	Knockdown of Brahma exacerbates Yki-mediated tissue overgrowth.	[33]
	BAP knockdown increases Yki target expression.	[33]
	TAZ/BRM interact via PPXY-WW domains to increase TAZ target expression.	[24]
SWI/SNF complex (indirect)	ACTL6A-p63 inhibits KIBRA expression to increase YAP activity.	[31]
	ARID1A sequesters YAP/TAZ from binding to TEAD to decrease YAP activity.	[34]
GAGA factor (direct)	GAF–Yki/dE2f1 bind to Yki targets, increasing their expression and overall cell proliferation.	[28]
	GAF ChIP-seq peaks overlap with Yki ChIP-seq peaks.	[30]
	Yki–GAF interactions occur in a WW domain-independent manner.	[30]
Mediator complex (direct)	Mediator–Yki interact in the nucleus and increase Yki target transcription.	[30]
Histone methyltransferase complex (direct)	Ncoa6–Yki/Sd interact via PPXY-WW domains at Yki targets to drive transcription.	[25,26]
	NCOA6–YAP interact and increase YAP target gene transcription.	[26]
NuRD complex (direct)	YAP/TAZ/TEAD–NuRD interact within the TSO complex to buffer/inhibit expression of pluripotency/ME specification genes.	[23]
	YAP/TAZ/TEAD–NuRD interact to epigenetically repress target gene activity to promote proliferation.	[27]

Note: For full names of gene symbols, see Abbreviations list at the end of this article.