lin-32 appears to function in a switch between certain hypodermal and neuronal cell fates. The recessive
lin-32(
e1926)X mutation transforms the Q, postdeirid or ray neuroblasts into specific hypodermal (seam/syncytial) cells (see CSH C. elegans Meeting Abstracts, 1983). Each neuroblast adopts a hypodermal fate normally assumed by cells with similar lineage histories. V5.pa (postdeirid neuroblast) becomes a seam cell; as does its sister and its Vn.pa lineal analogues. Each Rn.a cell (ray neuroblast) produces an anterior daughter that fuses with the
hyp-7 syncytium, and a posterior daughter that assumes the fate of its aunt (R1-R5: tail seam cells; R6- R9:
hyp-7 nuclei). Q usually fuses with
hyp-7, but at a lower frequency it divides to produce two
hyp-7 daughters, or becomes a seam cell.
e1926 does not appear to alter the H2.aa and T.p neurons and support cells. We have isolated a (recessive) deficiency, eDf17, that fails to complement
lin-32(
e1926). In
e1926/eDf17 animals, postembryonic development resembles that of
e1926 homozygotes, although Q more frequently becomes a seam. In addition, a second, embryonic, phenotype (this Newsletter) is more frequently expressed. These findings suggest that
e1926 reduces but does not eliminate gene activity. The phenotype of animals with reduced
lin-32 levels indicates that three types of controls operate to specify the fates of these lateral hypodermal cells. When
lin-32 levels are low, one control system specifies alternative hypodermal cell fates. A second system, involving
lin-32, creates 'neuroblast slots'. A third type determines whether these neuroblasts adopt Q, postdeirid, or ray fates. We wish to understand how the system that specifies hypodermal cell fates is related to the system that specifies neuronal cell fates. To what extent are they independent of one another? The mechanisms that specify particular neuroblast and hypodermal cell fates must differ by more than simply
lin-32 activity. When lin- 32 levels are low in otherwise wild type animals or in
lin-28(
n719) mutants. V5.pa and often Q become seam cells. However, if
lin-32 functions, these cells can adopt any of three different neuroblast fates. In the wild type, Q becomes a Q neuroblast and V5.pa becomes a postdeirid. In
lin-28(
n719) animals, V5.pa becomes a ray. [
lin28(
n719) was isolated and characterized by Victor Ambros; see Newsletter. Vol. 7 no. 2] These observations also indicate that the instructions that dictate a particular cell's neuroblast fate when
lin-32 is active can be changed without changing the instructions that dictate its hypodermal fate when
lin-32 levels are low. The heterochronic
lin-28(
n719) mutation mentioned above shifts the neuroblast fate of V5.pa from postdeirid to ray, but it does not alter the hypodermal fate associated with V5.pa in
lin-32 animals. If the hypodermal fate that normally underlies the ray were also shifted into the V5.pa lineal position, then in lin- 28
(n719);
lin-32(
e1926) animals, V5.pa should have generated only
hyp-7 syncytial and possibly tail seam cells. In addition to the neuroblast transformation,
lin-28(
n719) also causes the precocious expression of S3 hypodermal lineage sequences ( those normally expressed in the L3) during the L2. V(1-4).p and often V5.p divide once to produce seam and
hyp-7 daughters, as in the wild type L3. This suggests a simple explanation for the apparent sexual transformation in
lin-28 mutants. The decisions determining (i) hypodermal cell fates. (ii) the
lin-32-dependent creation of a neuroblast slot. and (iii) neuroblast fates may each be stage specific and under the control of certain heterochronic genes. We propose that in either sex, any
lin-32-derived S1 neuroblasts will adopt O fates, S2 neuroblasts will become postdeirids, and S3/4 neuroblasts will become rays. Wild type hermaphrodites may lack rays simply because
lin-32 levels are low during L3/4, and no such neuroblast is generated. Rays in
lin-28(
n719) hermaphrodites may result from incomplete heterochronic transformations that shift the S3/4 neuroblast program but fail to block the creation of the S2 V5.pa neuroblast slot. [see Figure 1]