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Published online November 5, 2007
doi:10.1083/jcb.200708205
The Journal of Cell Biology, Vol. 179, No. 3, 467-483
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Loewen et al.
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Article

 Inheritance of cortical ER in yeast is required for normal septin organization

Christopher J.R. Loewen1,2,3, Barry P. Young2,3, Shabnam Tavassoli2,3, and Timothy P. Levine1

1 Division of Cell Biology, University College London Institute of Ophthalmology, London EC1V 9EL, England, UK
2 Department of Cellular and Physiological Sciences and 3 Brain Research Centre, Life Sciences Institute, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada

Correspondence to Timothy P. Levine: tim.levine{at}ucl.ac.uk

How cells monitor the distribution of organelles is largely unknown. In budding yeast, the largest subdomain of the endoplasmic reticulum (ER) is a network of cortical ER (cER) that adheres to the plasma membrane. Delivery of cER from mother cells to buds, which is termed cER inheritance, occurs as an orderly process early in budding. We find that cER inheritance is defective in cells lacking Scs2, a yeast homologue of the integral ER membrane protein VAP (vesicle-associated membrane protein–associated protein) conserved in all eukaryotes. Scs2 and human VAP both target yeast bud tips, suggesting a conserved action of VAP in attaching ER to sites of polarized growth. In addition, the loss of either Scs2 or Ice2 (another protein involved in cER inheritance) perturbs septin assembly at the bud neck. This perturbation leads to a delay in the transition through G2, activating the Saccharomyces wee1 kinase (Swe1) and the morphogenesis checkpoint. Thus, we identify a mechanism involved in sensing the distribution of ER.

Abbreviations used in this paper: cER, cortical ER; HU, hydroxyurea; SGA, synthetic genetic array; TMD, transmembrane domain; VAP, vesicle-associated membrane protein–associated protein.


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