Skip to content
Login Register

#counting factor

2 public questions tagged with this topic.

Dictyostelium

Counting factor mutation (smlA-) leads to:

SmlA functions as negative regulator of counting factor production. In smlA null cells, countin and associated cf proteins accumulate to supranormal levels in conditioned medium, causing premature fragmentation of aggregation streams. Cells interpret elevated CF as indicator that aggregate is already too large, triggering increased random motility and reduced adhesion that breaks territories into numerous small mounds. Resulting fruiting bodies are diminutive with fewer spores each, though total spore number remains similar. This phenotype demonstrated counting factor as size-regulating quorum substance and revealed smlA role analogous to brake preventing overproduction, thereby fine-tuning optimal multicellular group dimensions for developmental success.

Ref: PNAS, Counting factor complex and smlA- mutants - overproduction leading to smaller aggregates.

View Details
Fertilization in mammals-lll

Counting factor (smlA) regulates:

Dictyostelium aggregation field size is regulated by autocrine factor called counting factor, identified as smlA secreted glycoprotein complex. It functions as quorum sensor: secreted by starving cells, concentration proportional to cell density modulates adhesion and motility via altering gene expression of adhesion molecules and myosin. High counting factor promotes breakup of streams into smaller aggregates; low promotes larger mounds. Mutants lacking smlA form abnormally large aggregates that produce oversized fruiting bodies, while overexpression yields tiny aggregates. Hence smlA regulates aggregate size ensuring optimal spore-stalk ratio and efficient dispersal rather than directly controlling motility or germination per se.

Ref: Jang & Gomer, Microbiology 2011: Counting factor smlA autocrine regulator of aggregate size in Dictyostelium.

View Details