|
|
|
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
First published online 23 June 2005
doi: 10.1242/dev.01916
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Cell and Developmental Biology, Vanderbilt University School of
Medicine, 465 21st Avenue South, Nashville, TN 37232, USA
2 Electron Microscopy Laboratory, University of California, Berkeley, 26
Giannini Hall, Berkeley, CA 94720-3330, USA
3 Department of Molecular Physiology and Biophysics, Vanderbilt University
School of Medicine, 465 21st Avenue South, Nashville, TN 37232, USA
* Author for correspondence (e-mail: david.greenstein{at}vanderbilt.edu)
Accepted 23 May 2005
The major sperm protein (MSP) is the central cytoskeletal element required for actin-independent motility of nematode spermatozoa. MSP has a dual role in Caenorhabditis elegans reproduction, functioning as a hormone for both oocyte meiotic maturation and ovarian muscle contraction. The identification of the signaling function of MSP raised the question, how do spermatozoa, which are devoid of ribosomes, ER and Golgi, release a cytoplasmic protein lacking a signal sequence? Here, we provide evidence that MSP export occurs by the budding of novel vesicles that have both inner and outer membranes with MSP sandwiched in between. MSP vesicles are apparently labile structures that generate long-range MSP gradients for signaling at the oocyte cell surface. Both spermatozoa and non-motile spermatids bud MSP vesicles, but their stability and signaling properties differ. Budding protrusions from the cell body contain MSP, but not the MSD proteins, which counteract MSP filament assembly. We propose that MSP generates the protrusive force for its own vesicular export.
Key words: Oogenesis, Meiotic maturation, Gamete interactions, Major sperm protein signaling, Vesicle budding, Unconventional protein secretion
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati 
Twitter What's this?
Related articles in Development:
This article has been cited by other articles:
|
|
 |
|
  J. A. Govindan, S. Nadarajan, S. Kim, T. A. Starich, and D. Greenstein Somatic cAMP signaling regulates MSP-dependent oocyte growth and meiotic maturation in C. elegans Development, July 1, 2009; 136(13): 2211 - 2221. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. M. Alcazar, R. Lin, and A. Z. Fire Transmission Dynamics of Heritable Silencing Induced by Double-Stranded RNA in Caenorhabditis elegans Genetics, November 1, 2008; 180(3): 1275 - 1288. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Chai, J. Withers, Y. H. Koh, K. Parry, H. Bao, B. Zhang, V. Budnik, and G. Pennetta hVAPB, the causative gene of a heterogeneous group of motor neuron diseases in humans, is functionally interchangeable with its Drosophila homologue DVAP-33A at the neuromuscular junction Hum. Mol. Genet., January 15, 2008; 17(2): 266 - 280. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M.-H. Lee, M. Ohmachi, S. Arur, S. Nayak, R. Francis, D. Church, E. Lambie, and T. Schedl Multiple Functions and Dynamic Activation of MPK-1 Extracellular Signal-Regulated Kinase Signaling in Caenorhabditis elegans Germline Development Genetics, December 1, 2007; 177(4): 2039 - 2062. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Corrigan, R. Subramanian, and M. A. Miller Eph and NMDA receptors control Ca2+/calmodulin-dependent protein kinase II activation during C. elegans oocyte meiotic maturation Development, December 1, 2005; 132(23): 5225 - 5237. [Abstract] [Full Text] [PDF]
|
|
