# A Novel Sucrose-Regulatory MADS-Box Transcription Factor GmNMHC5 Promotes Root Development and Nodulation in Soybean (Glycine max [L.] Merr.)

## TL;DR

This study identifies a soybean gene, GmNMHC5, that promotes root and nodule development and responds to sucrose signals.

## Contribution

The paper discovers a novel MADS-box transcription factor in soybean that regulates root and nodule growth in response to sucrose.

## Key findings

- GmNMHC5 is highly expressed in roots and nodules and is upregulated under short-day conditions.
- Overexpression of GmNMHC5 enhances lateral root development and nodule formation in soybean.
- GmNMHC5 is activated by exogenous sucrose, suggesting it senses and responds to sugar signals.

## Abstract

The MADS-box protein family includes many transcription factors that have a conserved DNA-binding MADS-box domain. The proteins in this family were originally recognized to play prominent roles in floral development. Recent findings, especially with regard to the regulatory roles of the AGL17 subfamily in root development, have greatly broadened their known functions. In this study, a gene from soybean (Glycine max [L.] Merr.), GmNMHC5, was cloned from the Zigongdongdou cultivar and identified as a member of the AGL17 subfamily. Real-time fluorescence quantitative PCR analysis showed that GmNMHC5 was expressed at much higher levels in roots and nodules than in other organs. The activation of expression was first examined in leaves and roots, followed by shoot apexes. GmNMHC5 expression levels rose sharply when the plants were treated under short-day conditions (SD) and started to pod, whereas low levels were maintained in non-podding plants under long-day conditions (LD). Furthermore, overexpression of GmNMHC5 in transgenic soybean significantly promoted lateral root development and nodule building. Moreover, GmNMHC5 is upregulated by exogenous sucrose. These results indicate that GmNMHC5 can sense the sucrose signal and plays significant roles in lateral root development and nodule building.