TY - JOUR
T1 - Hrp48 attenuates Sxl expression to allow for proper notch expression and signaling in wing development
AU - Suissa, Yaron
AU - Kalifa, Yossi
AU - Dinur, Tama
AU - Graham, Patricia
AU - Deshpande, Girish
AU - Schedl, Paul
AU - Gerlitz, Offer
PY - 2010/4/13
Y1 - 2010/4/13
N2 - Different signaling pathways are deployed in specific developmental contexts to generate sexually dimorphic traits. Recently, Sex-lethal (Sxl), the female determinant in Drosophila melanogaster, was shown to down-regulate Notch (N) signaling to accomplish sex-specific patterning. Paradoxically, however, both Sxl and N are ubiquitously expressed in all of the female cells. This raises a key question as to how, during monomorphic female development, N signaling escapes the negative impact of Sxl. Here, we uncover a regulatory loop involving Hrp48, an abundant Drosophila hnRNP, Sxl and N. Phenotypic consequences of the partial loss of hrp48 resemble that of N but are more pronounced in females than in males. Likewise, N levels are drastically diminished only in females. Interestingly, monomorphic female tissues including wing, eye and antennal discs display considerable increase in Sxl amounts. Finally, female-specific attenuation of N signaling is rescued upon simultaneous removal of Sxl. Thus, our data demonstrate that in monomorphic contexts, Hrp48 functions as a moderator of Sxl expression to achieve adequate levels of N receptor production and signaling. We propose that it is critical to modulate the activities of the master determinant underling sexual dimorphism, to ensure that it does not function inappropriately in monomorphic tissues and disrupt their development.
AB - Different signaling pathways are deployed in specific developmental contexts to generate sexually dimorphic traits. Recently, Sex-lethal (Sxl), the female determinant in Drosophila melanogaster, was shown to down-regulate Notch (N) signaling to accomplish sex-specific patterning. Paradoxically, however, both Sxl and N are ubiquitously expressed in all of the female cells. This raises a key question as to how, during monomorphic female development, N signaling escapes the negative impact of Sxl. Here, we uncover a regulatory loop involving Hrp48, an abundant Drosophila hnRNP, Sxl and N. Phenotypic consequences of the partial loss of hrp48 resemble that of N but are more pronounced in females than in males. Likewise, N levels are drastically diminished only in females. Interestingly, monomorphic female tissues including wing, eye and antennal discs display considerable increase in Sxl amounts. Finally, female-specific attenuation of N signaling is rescued upon simultaneous removal of Sxl. Thus, our data demonstrate that in monomorphic contexts, Hrp48 functions as a moderator of Sxl expression to achieve adequate levels of N receptor production and signaling. We propose that it is critical to modulate the activities of the master determinant underling sexual dimorphism, to ensure that it does not function inappropriately in monomorphic tissues and disrupt their development.
KW - Dosage compensation
KW - Sex determination
UR - http://www.scopus.com/inward/record.url?scp=77951058232&partnerID=8YFLogxK
U2 - 10.1073/pnas.0910570107
DO - 10.1073/pnas.0910570107
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C2 - 20351283
AN - SCOPUS:77951058232
SN - 0027-8424
VL - 107
SP - 6930
EP - 6935
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 15
ER -