Worm Breeder's Gazette 11(1): 53

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

Ectopic Mitosis in the Germline of lin-12(0) and WT Hermaphrodites

Geraldine Seydoux, Tim Schedl and Iva Greenwald

In lin-12(0) hermaphrodites, proximal germ cells fail to enter 
meiosis and instead proliferate in the mitotic cycle as distal germ 
cells do.  Meiosis and gametogenesis are observed only in the loop 
region where both oocytes and sperm are formed (WBG 10(1):108).  
Mosaic analysis has shown that lin-12 function is required in the 
somatic gonad to prevent proximal mitosis (WBG 10(2):82).  One 
possibility is that in lin-12(0) hermaphrodites, a cell in the 
proximal part of the somatic gonad promotes mitosis in the germline, a 
role normally associated only with the distal tip cell (DTC).  
Ablation of such a cell would restore meiosis proximally in lin-12(0) 
hermaphrodites.  Indeed, we have found that ablation of all anchor 
cells (ACs) restores proximal meiosis in lin-12(0) [unc-36(e251)lin-12(
n941)] hermaphrodites.  Conversely, ablation of all somatic gonadal 
cells except for the DTCs and one AC results in a gonad with proximal 
mitosis.  Thus, an AC is both necessary and sufficient to promote 
proximal mitosis in lin-12(0) hermaphrodites.  In addition, we have 
found that even in wild type, an AC can promote proximal germline 
mitosis when certain of its somatic neighbors Z1.p(a/p) and Z4.a(a/p) 
descendants] are ablated.
We conclude that, in wild type, cell-cell interactions among certain 
Z1.p(a/p) and Z4.a(a/p) descendants are necessary to keep the AC from 
promoting proximal mitosis in the germline.  Since proximal mitosis is 
observed in lin-12(0) mutants, we infer that these cell-cell 
interactions require lin-12 activity.
Keeping in mind that the AC is in close contact with proximal germ 
cells at least up to the L2 molt, we propose two models to account for 
our findings.  In one model, we postulate that cell-cell interactions 
prevent the AC from expressing the 'DTC-to-germline' signal.  Either 
ablation of somatic cells neighboring the AC or removal of lin-12 
activity would result in the expression of the 'DTC-to-germline' 
signal by the AC, which would promote mitosis in proximal germ cells.
Another model relies on the proposal that lin-12 functions as the 
receptor for the 'AC-to-VU' signal, which emanates from the 
presumptive AC (Seydoux and Greenwald, 1989) and that glp-1 functions 
as the receptor for the 'DTC-to-germline' signal (Austin and Kimble, 
1987; Yochem and Greenwald, 1989).  In view of the functional and 
molecular similarities between lin-12 and glp-1 (see Yochem and 
Greenwald, 1989), we postulate that the 'AC-to-VU' signal can activate 
glp-1 in germ cells.  In wild type, the 'AC-to-VU' signal 
preferentially binds to lin-12 and not glp-1.  In lin-12(0) 
hermaphrodites, however, the 'AC-to-VU' signal is available to 
activate glp-1 and promote mitosis in proximal germ cells.  Similarly, 
in operated wild type hermaphrodites in which cells we hypothesize are 
expressing lin-12 have been ablated, the 'AC-to-VU' signal can 
activate glp-1 in proximal germ cells.
We are currently testing the requirement for glp-1 for the proximal 
mitosis observed in operated lin-12(+) hermaphrodites by repeating our 
ablation experiments in glp-1(ts) animals.  We are also reverting the 
lin-12(0) germline defect to help us distinguish between different 
models and perhaps to define the 'AC-to-VU' signal.