blmp-1 : ham-3

LDB-1 and HAM-3 bind to BLMP-1.

blmp-1 : ldb-1

LDB-1 and HAM-3 bind to BLMP-1.

ham-1 : pig-1

The PIG-1::GFP fluorescence was visible in all the WT Q.a cells, but was significantly reduced in ham-1 mutants. PIG-1::GFP fluorescence did not change in neighboring seam cells of ham-1 mutants.

ham-1 : pig-1

The PIG-1::GFP fluorescence was visible in all the WT Q.a cells, but was significantly reduced in ham-1 mutants. PIG-1::GFP fluorescence did not change in neighboring seam cells of ham-1 mutants.

Interaction involving ced-3

"In ham-1 mutants, the HSN/PHB neuroblast divides symmetrically, inappropriately generating two HSN/PHB precursor cells, and subsequently, extra HSN and PHB neurons. This phenotype can be seen using srb6::gfp, where PHB neuron duplications generate extra GFP-expressing phasmid neurons about 25% of the time in ham-1 mutants (Table 1). In ham-1 ced-3 double mutants, the phenotype is more striking (Table 1)."

ham-1 : lin-32

lin-32(cas21), or ham-1(gm279) single mutation causes two-A/PQR neuron phenotype with the penetrance of 46%, and 72% respectively. However, in lin- 32(cas21); ham-1(gm279) double mutants, we showed that the two-A/PQR phenotype is significantly enhanced to 92%, suggesting that LIN-32 functions in parallel with the HAM-1/PIG-1 pathway in regulating Q.a lineage progression.

Interaction involving ham-1

"In ham-1 mutants, the HSN/PHB neuroblast divides symmetrically, inappropriately generating two HSN/PHB precursor cells, and subsequently, extra HSN and PHB neurons. This phenotype can be seen using srb6::gfp, where PHB neuron duplications generate extra GFP-expressing phasmid neurons about 25% of the time in ham-1 mutants (Table 1). In ham-1 ced-3 double mutants, the phenotype is more striking (Table 1)."

lin-32 : pig-1

lin-32(cas21), or pig-1(gm344) single mutation causes two-A/PQR neuron phenotype with the pene- trance of 46%, or 19% respectively. However, in lin-32(cas21); pig-1(gm344) double mutants, we showed that the two-A/PQR phenotype is significantly enhanced to 83%, suggesting that LIN-32 functions in parallel with the HAM-1/PIG-1 pathway in regulating Q.a lineage progression.