Worm Breeder's Gazette 11(3): 47

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.

The lin-14 Gene Appears to Code for Two Proteins, One of Which Accumulates Predominantly in Seam Cell Nuclei

Bruce Wightman, Prema Arasu and Gary Ruvkun

The lin-14 gene produces two transcripts that apparently encode 
proteins that differ from each other at the N-terminus (see Burglin, 
et al., WBG, this issue).  Transcript A splices exon 4 to exon 5, 
while transcript B splices exons 1, 2, and 3 directly to exon 5.  We 
used RNA probes specific for exons 3, 4, and 5 in order to analyze by 
RNAase protection the regulation of these two transcripts in staged N2 
animals and various mutants.  In addition, we used anti-lin-14 
antibody staining to assess whether the product of the lin-14A 
transcript is expressed in distinct cell lineages or cell types, or at 
distinct times during development.  Transcript B is present in about 
three-fold greater abundance than transcript A, consistent with their 
representation in the cDNA library.  This ratio does not change 
detectably at any post-embryonic stage (the jury is still out on 
relative embryonic expression).  During post-embryonic development, 
both transcripts are expressed at highest levels (about 1/50 myo-1 ) 
at L1.  Both transcripts coordinately decrease in abundance from L2 to 
adult stages when the level is about 10% L1 abundance, even though no 
protein is detectable at these stages.  One recessive mutant, lin-14(
n360), specifically affects transcript B only.  Transcript B is almost 
entirely absent in this mutant, while transcript A is unaffected.  
This result is consistent with the observation that n360 is associated 
with an allele-specific RFLP in the genomic fragment containing exon 
Since n360 animals express almost no transcript B, we could observe 
the temporal and spatial regulation of lin-14 protein accumulations 
from transcript A.  n360 L1 larvae were stained with a polyclonal anti-
lin-14 antibody.  All hypodermal seam cell and hyp5 nuclei stain 
intensely, while hyp7, P cells, neurons, body muscle, and intestinal 
nuclei stain very faintly.  All these nuclei stain intensely at this 
stage in wild-type.  Since most of the lin-14 protein present must be 
produced from transcript A, most of the observed staining must be lin-
14A product.  Therefore, we propose that lin-14A product is expressed 
predominantly in the hypodermal seam, while lin-14B product is 
expressed in a variety of cell types.  We are attempting to make 
antibodies which are specific to the N-terminus of each of the two 
proteins to confirm these observations.  n360 is a lin-14 a+b- mutant 
as determined genetically by Ambros and Horvitz (1987): seam cells 
execute normal L1 hypodermal cell fates, but execute precocious fates 
at L2 and later stages, while lin-14 a-b- alleles execute precocious 
fates at all postembryonic stages.  Our molecular analysis of n360 
indicates that lin-14b genetic function is encoded by the lin-14B 
transcript (what a coincidence).  The antibody staining results 
suggest that L1 seam cell fates are normal in n360 because lin-14A 
protein accumulates at normal levels in the hypodermal seam.  Later 
fates in the seam are precocious in n360 because either they require 
non-autonomous interactions dependent on lin-14B expression in other 
tissues, or because they are dependent on lin-14B expression in the 
seam, or even more complicated schemes.  Because the lin-14A protein 
accumulates in the same set of cell nuclei whose fates are controlled 
by the lin-14a gene activity, it is likely that the lin-14a gene 
activity is cell autonomous.  Although hypodermal cell fates are 
normal at L1 in n360 animals, these mutants form precocious L1 dauers 
like other lin-14 mutants (Liu and Ambros, G&D 3:2039).  Our results 
indicate that while accumulation of lin-14A protein in the seam is 
sufficient to specify L1 cell lineages in those cells, it is not 
sufficient to block L1 dauer formation.  This suggests that temporal 
control of dauer formation is dependent on the level of lin-14B 
protein in cells other than the hypodermal seam (neurons?).  While lin-
14A and lin-14B transcripts have similar temporal expression profiles, 
their products differ in their cellular pattern of expression.  It is 
likely that the two transcripts are derived from separate promoters, 
so cell type-specific cis-acting regulatory sites may be present in 
the two promoters.  In addition, we expect that the distinct lin-14 
proteins produced in each of these cell types will specify different 
cell fates.