let-99 Antibody

Molecular Role of LET-99

LET-99 is a cortically localized protein that regulates spindle positioning and cortical pulling forces during asymmetric cell division. It forms a band-like structure at the posterior-lateral cortex, which:

• Inhibits GPR-1/2 and LIN-5 localization, reducing lateral-posterior pulling forces to enable proper spindle rotation and positioning .

• Coordinates with PAR-1 kinase to establish force asymmetry, critical for partitioning fate determinants in early embryos .

Mechanism in Cytokinesis

In symmetrically and asymmetrically dividing cells, LET-99 contributes to contractile ring formation by:

• Enriching non-muscle myosin II (NMY-2) at the cleavage furrow .

• Acting independently of the centralspindlin complex or anillin, suggesting a parallel pathway for furrow ingression .

Table 1: Functional Comparison of LET-99 in Cell Division

Genetic and Laser Ablation Studies

• let-99 mutants exhibit defective spindle rotation and asymmetric force distribution, leading to misplaced cleavage furrows .

• Severing the central spindle in let-99 mutants reduces posterior spindle pole velocity by 35%, confirming its role in force regulation .

Evolutionary and Mechanistic Insights

LET-99’s function is conserved in regulating cortical force generators. Its inhibition of Gα signaling provides a model for how polarity cues translate into mechanical asymmetry during division .

Research Applications and Gaps

While LET-99 antibodies are not commercially characterized, studies utilize genetic tools (e.g., RNAi, mutants) to probe its function. For example:

• Laser ablation assays quantify spindle pole velocities to infer force imbalances .

• Fluorescent reporters track NMY-2 localization in let-99 embryos .

Comparative Context: CD99 Antibodies

Though unrelated to LET-99, CD99 antibodies (e.g., AF3968) are well-documented in human research, highlighting the importance of target-specific validation .