A search for genes that are synthetic with
lin-35/Rb, a retinoblastoma protein homolog in C.elegans, led to the identification of
pha-1 and
ubc-18 along with several other genes (1). Strains carrying mutations in either
pha-1(
fd1) or
ubc-18(
ku354) were viable with no obvious morphological phenotypes. Whereas,
lin-35;
pha-1(
fd1) and
lin-35;
ubc-18 double mutants arrested at the early larval stages with severe pharyngeal morphological defects and Pun (Pharynx UNattached) phenotypes. Extensive analysis of these double mutants suggested redundant roles for
pha-1,
lin-35 and
ubc-18 during early stages of pharyngeal morphogenesis (2). Furthermore, earlier studies by Schnabel implicated
pha-1 to act independently during other aspects of pharyngeal development (3).
sup-36 and
sup-37 are two previously identified extragenic mutations that suppresses the strong LOF of
pha-1 (4). Interestingly,
sup-36 and
sup-37 mutations also suppress the synthetic phenotypes of
lin-35;
pha-1(
fd1),
lin-35;
ubc-18,
ubc-18;
pha-1(
e2123)(16oC) and
lin-35;
pha-1(
e2123)(16oC) double mutants, further suggesting that
pha-1 functions in parallel with
lin-35 and
ubc-18 in regulating a common target. Hence, identifying
sup-36 and
sup-37 would shed more light on the understanding the role of PHA-1, UBC-18 and LIN-35 in pharyngeal development. Towards this,
sup-36 was mapped to chromosome IV between nucleotides 6414194 and 6649293 and
sup-37 was mapped to chromosome V between nucleotides 8601984 and 8925122. Currently, efforts are underway to clone
sup-36 and
sup-37 using fosmids from the mapped region. However, we have thus far been unable to obtain clear rescue. For this reason, the identification of the suppressors using
mos1-mediated mutagenesis approach has also been initiated and the results will be reported.