Na+, K+/H+ antiporters regulate the pH of endoplasmic reticulum and auxin‐mediated development. (23rd February 2018)

• Record Type: Journal Article
• Authors: Fan, Ligang; Zhao, Lei; Hu, Wei; Li, Weina; Novák, Ondřej; Strnad, Miroslav; Simon, Sibu; Friml, Jiří; Shen, Jinbo; Jiang, Liwen; Qiu, Quan‐Sheng
• Is Part Of: Plant, cell and environment. Volume 41:Number 4(2018)
• Page Start: 850
• Page End: 864
• Publication Date: 2018-02-23
• Subjects: Arabidopsis -- endosomal Na+, K+/H+ antiporters -- AtNHX5 -- AtNHX6 -- PIN5 -- pH; Plant physiology -- Periodicals; Plant cells and tissues -- Periodicals; Plant communities -- Periodicals; 581.105
• DOI: 10.1111/pce.13153
• Languages: English
• ISSNs: 0140-7791

Abstract

Abstract: AtNHX5 and AtNHX6 are endosomal Na +, K + /H + antiporters that are critical for growth and development in Arabidopsis, but the mechanism behind their action remains unknown. Here, we report that AtNHX5 and AtNHX6, functioning as H + leak, control auxin homeostasis and auxin‐mediated development. We found that nhx5 nhx6 exhibited growth variations of auxin‐related defects. We further showed that nhx5 nhx6 was affected in auxin homeostasis. Genetic analysis showed that AtNHX5 and AtNHX6 were required for the function of the endoplasmic reticulum (ER)‐localized auxin transporter PIN5. Although AtNHX5 and AtNHX6 were colocalized with PIN5 at ER, they did not interact directly. Instead, the conserved acidic residues in AtNHX5 and AtNHX6, which are essential for exchange activity, were required for PIN5 function. AtNHX5 and AtNHX6 regulated the pH in ER. Overall, AtNHX5 and AtNHX6 may regulate auxin transport across the ER via the pH gradient created by their transport activity. H + ‐leak pathway provides a fine‐tuning mechanism that controls cellular auxin fluxes. Abstract : This study aims to understand the mechanism underlying the function of the endosomal antiporters AtNHX5 and AtNHX6 in controlling plant development. We observed the auxin‐related growth defects and auxin homeostasis alterations in nhx5 nhx6 double mutants, which led to the discovery of the involvement of AtNHX5 and AtNHX6 in the function of the endoplasmic reticulum‐localized auxin transporter PIN5. We demonstrated that AtNHX5 and AtNHX6 might regulate auxin transport across the endoplasmic reticulum via the pH gradient created by their transport activity. This study highlights the importance of AtNHX5 and AtNHX6, functioning as H + leak, in controlling auxin homeostasis and auxin‐mediated development.