Lack of Effect of Microfilament or Microtubule Cytoskeleton-Disrupting Agents on Restriction of Externalized Phosphatidylserine to Rod Photoreceptor Outer Segment Tips

  • Linda Ruggiero
  • Silvia C. FinnemannEmail author
Conference paper
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 801)


In the mammalian retina, life-long renewal of rod photoreceptor outer segments involves circadian shedding of distal outer segment tips and their prompt phagocytosis by the adjacent retinal pigment epithelium (RPE) every morning after light onset. Failure of this process causes retinal dystrophy in animal models and its decline likely contributes to retinal aging and some forms of degeneration of the human retina. We previously found that surface exposure of the membrane phospholipid phosphatidylserine (PS) is restricted to outer segment tips with discrete boundaries in mouse retina and that both frequency and length of tips exposing PS peak after light onset. Here, we sought to test mechanisms photoreceptors use to restrict PS specifically to their outer segment tips. To this end, we tested whether nocodazole or cytochalasin D, perturbing microtubule or F-actin microfilament cytoskeleton, respectively, affect localization of externalized PS at outer segment tips. Fluorescence imaging of PS exposed by rods in freshly dissected, live mouse retina showed normal PS demarcation of outer segment tips regardless of drug treatment. These results suggest that the mechanism that restricts externalized PS to rod tips is independent of F-actin and microtubule cytoskeletal systems.


Actin Cytoskeleton Microtubules Outer segment Phosphatidylserine Photoreceptor Retina Shedding 



Hank’s buffered saline solution




Polarity-sensitive indicator of viability and apoptosis


Photoreceptor outer segments


Retinal pigment epithelium



We are grateful for the Young Investigator Travel Award from the National Eye Institute that supported the participation at the RD2012 Symposium of Linda Ruggiero. We thank all members of the Finnemann lab for helpful discussions. This study was supported by NIH grant EY13295.


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Copyright information

© Springer Science+Business Media, LLC 2014

Authors and Affiliations

  1. 1.Department of Biological Sciences, Center for Cancer, Genetic Diseases, and Gene RegulationFordham UniversityBronxUSA

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