Septum formation in the desmid Xanthidium (Chlorophyta): Effects of cytochalasin D and latrunculin B suggest the involvement of actin microfilaments

Citation
M. Hoftberger et U. Lutz-meindl, Septum formation in the desmid Xanthidium (Chlorophyta): Effects of cytochalasin D and latrunculin B suggest the involvement of actin microfilaments, J PHYCOLOGY, 35(4), 1999, pp. 768-777
Citations number
31
Categorie Soggetti
Aquatic Sciences
Journal title
JOURNAL OF PHYCOLOGY
ISSN journal
00223646 → ACNP
Volume
35
Issue
4
Year of publication
1999
Pages
768 - 777
Database
ISI
SICI code
0022-3646(199908)35:4<768:SFITDX>2.0.ZU;2-2
Abstract
Septum formation and mitosis were investigated by light and electron micros copical techniques as well as through the completion of inhibitor experimen ts in the unicellular desmid Xanthidium armatum (Breb.) Rabenh, In untreate d cells, numerous endoplasmic reticulum (ER) cisternae permeated the mitoti c apparatus and secretory vesicles, and ER formed a band in front of the li nearly growing septum, indicating the predetermined direction of septum gro wth, Under the influence of cytochalasin D (CD), the vesicle/ER band lost i ts proper orientation, which led to a malformed septum wall; moreover, abno rmal septum branches could potentially have developed. Whereas the septum o f an untreated cell only grew at its edge, the CD-induced branches (also wi th a vesicle/ER band in front) represented additional growing zones. These observations indicated that actin filaments were involved in establishing, maintaining, and orienting the "preforming" vesicle/ER band and, thus, the later septum. Latrunculin B (LB) had more severe effects on septum formatio n than did CD. Only small accumulations of septum material were found at th e septum edge, and no aberrant growth of the septum occurred in LB-treated as in CD-treated cells. This could be explained by the more rapid disturban ce of all actin-driven processes after LB treatment, which was assumed, bec ause even low concentrations of the drug rapidly inhibited cytoplasmic stre aming.