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.
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.