# Transcripts from the src-1(cj293) mutant can encode a SRC-1 molecule lacking the SH2 domain in Caenorhabditis elegans

## TL;DR

This study shows that a specific mutation in C. elegans produces a version of the SRC-1 protein missing a key domain, leading to overactivity in neurons.

## Contribution

The study confirms that the src-1(cj293) mutation generates a transcript lacking the SH2 domain, supporting its role as a constitutively active allele.

## Key findings

- RNA seq data shows the src-1(cj293) mutation leads to a splice between exon 3 and exon 6.
- The resulting transcript can encode a SRC-1 molecule missing the SH2 domain.
- This mutation causes overactive SRC-1 in VD neuron growth cones during outgrowth.

## Abstract

Previous studies suggest that the

src-1
(
cj293
)

mutation is an activated

src-1

allele in

C. elegans

with the potential to encode a molecule lacking the SH2 domain.

src-1
(
cj293
)

is a deletion with breakpoints in introns 3 and 5, deleting exons 4 and 5, which encode the SH2 domain. If exon 3 is spliced to exon 6, the reading frame is maintained. Here, RNA seq of

src-1
(
cj293
)

mutants showed that the exon 3 to exon 6 splice does not occur in

src-1
(+)

but is robustly present in

src-1
(
cj293
)

. Thus,

src-1
(
cj293
)

produces a transcript that can encode a
SRC-1
molecular lacking the SH2 domain, which leads to overactive
SRC-1
in growth cones of VD neurons during their outgrowth (
i.e.

src-1
(
cj293
)

might be a constitutively-active mutation).