Back

GDF3 simultaneously antagonizes BMP signaling and activates TGFβ receptor signaling

Ramachandran, D.; Kotikalapudi, N.; Maridas, D. E.; Gulko, A.; Tsai, L. T.; Rosen, V.; Banks, A. S.

2022-11-07 cell biology
10.1101/2022.11.07.515236 bioRxiv
Show abstract

Growth differentiation factor 3 (GDF3) is a relatively understudied member of the TGF{beta} superfamily that is highly expressed during development. However, the function of GDF3 in adult biology is contentious. We use in vivo approaches to show that GDF3 loss-of-function in adipose tissue of obese adult mice causes reduced body weight and improved whole-body insulin sensitivity. These effects are accompanied by altered regulation of genes targeted by the TGF{beta} superfamily in vivo. Using in vitro approaches, we show that GDF3 can influence both arms of the TGF{beta} superfamily: GDF3 simultaneously inhibits BMP signaling and activates activin-like SMAD 2/3 signaling. We identify the type II receptors mediating this activity. GDF3 binds to the type II receptors BMPR2, ACTRIIA and ACTRIIB and achieves dose-dependent inhibition of multiple BMP proteins including BMP2, BMP7, BMP9, BMP10, and BMP15 in vitro. We also find that GDF3 activates TGF{beta}/activin-like SMAD2/3 signaling. Unbiased expression profiling confirms that GDF3 both attenuates BMP2-regulated gene expression and drives TGF{beta}/activin-like gene expression. Together these results provide much needed clarity to both the molecular pathways involved in GDF3 signaling and the physiological effects of GDF3 loss of function.

Matching journals

The top 9 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.