Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.
Inhibition of Netrin-Mediated Axon Attraction by a Receptor Protein Tyrosine Phosphatase
Chieh Chang,1,2Timothy W. Yu,2Cornelia I. Bargmann,2*Marc Tessier-Lavigne1*
During axon guidance, the ventral guidance of the Caenorhabditiselegans anterior ventral microtubule axon is controlled by twocues, the UNC-6/netrin attractant recognized by the UNC-40/DCCreceptor and the SLT-1/slit repellent recognized by the SAX-3/roboreceptor. We show here that loss-of-function mutations in clr-1enhance netrin-dependent attraction, suppressing ventral guidancedefects in slt-1 mutants. clr-1 encodes a transmembrane receptorprotein tyrosine phosphatase (RPTP) that functions in AVM toinhibit signaling through the DCC family receptor UNC-40 andits effector, UNC-34/enabled. The known effects of other RPTPsin axon guidance could result from modulation of guidance receptorslike UNC-40/DCC.
1 Department of Biological Sciences, Howard Hughes Medical Institute (HHMI), Stanford University, Stanford, CA 94305, USA. 2 Department of Anatomy and Department of Biochemistry and Biophysics, HHMI, University of California San Francisco (UCSF), San Francisco, CA 94143, USA.
Present address: Genentech, Incorporated, 1 DNA Way, South SanFrancisco, CA 94080, USA.
* To whom correspondence should be addressed. E-mail: cori{at}itsa.ucsf.edu (C.I.B.); marcH{at}gene.com (M.T.L.)
Present address: Genentech, Incorporated, 1 DNA Way, South San Francisco, CA 94080, USA. 
