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abelson murine leukemia viral oncogene large tumor suppressor runt - related transcription factor peroxisome proliferator - activator receptor gamma 2 transcriptional enhancer activator domain yes - associated protein
based on a number of criteria , certain genes are categorized as oncogenes whereas the genes that oppose their function are regarded as tumor suppressors .
this categorization is of enormous value in investigating the molecular basis of cell fate determination . by and large ,
these genes are components or targets of cellular signaling pathways that transmit bimodal on and off instructions .
the extent to which this perception is correct forms the basis of our recent study .
we investigated the crosstalk between the dna damage response pathway and the hippo pathway and revealed that a proto - oncoprotein switched to behave as a tumor suppressor .
our finding therefore violates the on / off instruction rules by including a third option of opposing antipodal switching .
the transcriptional coactivator yes - associated protein ( yap ) enters the nucleus by default to target specific genes .
yap has been implicated as an oncogene in conjunction with the transcriptional enhancer activator domain ( tead ) family of transcription factors in human cancers , where it activates proproliferative and antiapoptotic target genes .
the activity of yap is blunted by blocking its nuclear entry through the hippo pathway , which is important in regulating cell contact inhibition , organ size control , and cancer development . under conditions of cell  cell contact , upstream elements of the hippo pathway transmit signals through the kinase large tumor suppressor ( lats ) , which phosphorylates yap on serine residues resulting in yap cytoplasmic sequestration , downregulation of its nuclear target genes , and compromised oncogenic potential .
a twist was introduced into this coherent picture when it was recognized that yap is also a coactivator of proapoptotic genes . in response to dna damage , yap targets p73 , a member of the tumor suppressor p53 family , to induce proapoptotic gene expression and initiate a cellular death axis .
the non - receptor tyrosine kinase abelson murine leukemia viral oncogene ( c - abl ) is activated under conditions of dna damage and phosphorylates tyrosine residues on both p73 and yap .
tyrosine phosphorylated yap promotes the death axis at 2 levels : by enhancing the p73-mediated death axis and by supporting p73 accumulation .
moreover , when coactivating the runt - related transcription factor ( runx ) , yap regulates the expression of itch , the p73 e3 ligase . upon tyrosine phosphorylation by c - abl ,
c - abl thus switches yap behavior from activating the e3 ligase that induces p73 degradation to coactivating the accumulated p73 .
this regulatory module exemplifies the capacity of c - abl to switch yap behavior to promote the opposing function .
a similar behavior was discovered at the level of targeting the tead transcription factor . the nuclear yap 
tead complex controls the survival axis by inducing transcription of a set of genes involved in 2 major activities : supporting cell proliferation on one hand and inhibiting apoptosis on the other hand .
these two yap - regulated activities give rise to a net increase in the cell population .
however , when c - abl is activated in response to dna damage , the tyrosine - phosphorylated yap still binds tead but is unable to induce the survival axis .
thus , as modified yap also induces the death axis via p73 , activated c - abl switches yap from being an oncogene to becoming a tumor suppressor ( fig .
these findings exemplify a newly emerging principle in signaling : not only turning on and off , but also dictating an opposing function . 

1.yap is switched from oncogene to tumor suppressor function through phosphorylation by c - abl .
( a ) when the hippo pathway is inactive , as in proliferating cells , yes - associated protein ( yap ) coactivates the transcriptional enhancer activator domain ( tead ) transcription factor to express survival genes involved in the suppression of apoptosis .
( b ) under dna damage conditions , abelson murine leukemia viral oncogene ( c - abl ) is activated and phosphorylates p73 and yap . these modifications lead to yap - p73 induced transcription of proapoptotic genes and activation of a death axis .
simultaneously , phosphorylation of yap by c - abl inhibits its potential to coactivate tead , resulting in blunting of the expression of antiapoptotic genes and promotion of apoptosis . 
 
yap is switched from oncogene to tumor suppressor function through phosphorylation by c - abl .
( a ) when the hippo pathway is inactive , as in proliferating cells , yes - associated protein ( yap ) coactivates the transcriptional enhancer activator domain ( tead ) transcription factor to express survival genes involved in the suppression of apoptosis .
( b ) under dna damage conditions , abelson murine leukemia viral oncogene ( c - abl ) is activated and phosphorylates p73 and yap . these modifications lead to yap - p73 induced transcription of proapoptotic genes and activation of a death axis . simultaneously , phosphorylation of yap by c - abl inhibits its potential to coactivate tead , resulting in blunting of the expression of antiapoptotic genes and promotion of apoptosis . at first
it may appear odd that a cell would use the same protein as an oncogene and as a tumor suppressor . what could be the advantage of one effector controlling 2 opposing tasks ?
recent studies revealed that il-2 exhibits paradoxical behavior in the determination of t - cell homeostasis . by applying a mathematical model
, it was demonstrated that a single secreted molecule makes the homeostasis more robust against perturbations . in our system
the hippo pathway turns yap effector activity on and off whereas the dna damage response switches yap activity to the opposing task .
knows what to do when receiving 2 schizophrenic instructions . we hypothesized that one instruction must be dominant over the other
. we found that when the hippo pathway is active , namely under cell  cell contact conditions , the dna damage response is inactivated .
this is accomplished by a double lock mechanism ; on one hand the hippo kinase lats neutralizes yap via its sequestration in the cytoplasm , while on the other hand it inhibits c - abl kinase activity .
the next question is why the hippo pathway is dominant over the dna damage response .
the hippo pathway is functional at the level of on / off in a reversible manner .
yap enters and exits the nucleus based on received instructions and does not reach a fixed irreversible status .
in contrast , c - abl is involved in irreversible nuclear processes , such as inducing the death axis activity of yap .
recently , we found that c - abl promotes adipocyte differentiation , another irreversible process , by phosphorylation of the key adipogenic transcription factor peroxisome proliferator - activator receptor gamma 2 ( ppar2 ) and its subsequent stabilization and activation .
it is therefore somewhat intuitive that the reversible processes would be dominant over the irreversible ones . in summary
, we attribute signaling to not only the capacity to turn downstream effectors on and off , but also the ability to impose an opposing task on a given effector .
the interplay between the hippo pathway and the dna damage response nicely exemplifies this principle .
in addition , we think that this model is important to reach rapid homeostasis , provided that the involved pathways are hierarchically designed .
551/11 ) , and from the minerva foundation with funding from the federal german ministry for education and research .
cancer research has been significantly accelerated by viewing cancer as a functional collision between 2 dichotomous sets of genes : oncogenes and tumor suppressors . 
 signaling pathways turn oncogenes and tumor suppressors on and off to dictate cell fate decisions . 
 we contend that signaling also dictates opposing behaviors of a given effector .