Worm Breeder's Gazette 10(3): 74

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.

Is Tc1 Transposition Regulated on the Transcriptional Level?

Luc L.M.G. Beckers and Ronald H.A. Plasterk

At the 1987 CSH worm meeting we reported that using Tc1 as a probe 
in Northern blot analysis, we observed a polyadenylated transcript in 
Bergerac but not in Bristol worms.  (This was confirmed by Radice, et. 
al., (WBG 10.2)).  These results have been extended and some 
conclusions can now be 
drawn:
(1)  The transcript (approximately 1,500 bases long) is found 
consistently only in strains that are active in Tc1 transposition.  
Controls have been done with overexposure of Northern blots of Bristol 
mRNA; blots were checked with an actin probe for quality and amount of 
RNA in the preps.  We feel sure that we are not just observing the 
result of a copy number difference of Tc1; the Tc1 homologous 
transcript is absent in Bristol.  The correlation between presence of 
the transcript and transpositional activity suggests that the secret 
of regulation of Tc1 activity is in Tc1 transcription regulation.  To 
determine the structure of the transcript, we made a cDNA library of 
RW7000 and selected Tc1 homologous clones.  Twenty were found and 
these are currently being analyzed.
(2)  The assumption that Tc1 transcription is essential for 
transposition is supported by the following:  It was previously 
reported by Carol Trent and Jonathan Hodgkin that a direct descendent 
of the sma-1 mutant CB30(e30) (which is derived from Bristol N2) had 
become active in transposition (abstract book 1987 CSH meeting).  The 
active derivative was renamed CB4000.  We looked at RNA of CB4000 and 
it contains a transcript of the same size as Bergerac, which is absent 
in the N2 strain.  This shows that the acquisition of transpositional 
activity is accompanied by the appearance of this transcript.
(3)  Somatic excision apparently is independent of Tc1 transcription,
because the Bristol strain contains no Tc1 homologous transcripts in 
somatic cells and still it shows somatic excision of Tc1.  If indeed 
Tc1 transcription is essential for germ-line transposition and 
excision of Tc1, then somatic excision of Tc1 must be a process that 
differs significantly from the germ-line events.
(4)  If the essence of the Bristol/Bergerac difference is in Tc1 
transcription, then the next question is what causes the difference in 
TcA expression.  This is the question that we are currently trying to 
answer.