Embryological aspects of leafhopper endosymbiosis
and their evolutionary implications: A review
Sander, K.
Institut für Biologie I (Zoologie), Hauptstr.1, D-79104 Freiburg, Germany
Paul Buchner, doyen of research on animal endocytobiosis, testified leafhoppers "a thoroughly confusing diversity of symbiotic devices". Among the lesser known aspects of this diversity are the ontogenetic mechanisms bringing it about. After a brief survey of such mechanisms and their evolutionary implications, based largely on the work of Buchner [1] and Müller [2], we shall review observations and experiments revealing interactions between host embryo and endocytobionts in the jassid leafhopper Euscelis incisus (formerly E. plebejus).
The Euscelis endocytobionts, classified by Müller as "a" and "t" symbionts, cycle twice from "infective" to "vegetative" morphs and back, each time shifting to new locations or host cells; they multiply considerably during early embryogenesis [3]. Multiplication is apparently controlled to some degree by the host embyo, because when the initial symbiont mass in the egg is very small, the subsequent increase will be far above average so that the definitive mycetomes can reach full size (W. Herrmann and K.Sander, unpubl.). The primary a-mycetocytes form close to the germline cells, which begs the question whether they are modifications of the latter. They bind anti-vasa antibody, a property specific to germline cells in many insects; however, the antibody binds also to some of the cells that later on harbour the symbionts in the definitive mycetomes (R. Schröder and K. Sander, unpubl.) and therefore the issue must remain open. Experimental dissection of embryogenesis [4] has shown that symbionts placed ectopically may transform adjacent blastoderm cells into primary a-mycetocytes but fail to induce any of the definitive cell types and organs that would harbour the symbionts later on. These cell types and their organ-forming properties apparently are encoded in the embryo's developmental program, because they appear and form organs in the absence of symbionts as well. Unexpected complications arise when the maternal symbionts are reduced or eliminated by tetracyclin. A detailed study (I.Barton and K.S.) revealed that the idling transmission mechanism in the ovarian follicle frequently causes structural anomalies at the posterior egg pole [6]. These - and not a shortage of transmitted symbionts - are likely to trigger the teratological effects described by Schwemmler et al. [7], because eggs with normal polar structure produce normal embryos even when supplied with only a tiny fraction of the normal symbiont mass [6].
[1] Buchner, P (1965) Endosymbiosis of Animals with Plant Microorganisms. Wiley-Interscience, New York
[2] Müller, H.J. (1962) Z. Morph. Ökol. Tiere 51:190-210
[3] Körner, H. (1976) Experientia 32:463
[4] Sander, K. (1968) Dev. Biol. 17:16-28
[5] Sander, K. (1977) Verh. Dtsch. Zool. Ges. 1977:306
[6] Sander, K. (1984) Adv. Invertebr. Reprod. 3:127-136
[7] Schwemmler, W. et al. (1973) Z. Morph. Tiere 74:297-322
| LOCATION |
DATE |
TIME |
| Lecture Hall I |
Thursday, April 9 |
08:55 am |