May 16, 2019
How one fern can soak up so much arsenic – and not die
WEST LAFAYETTE, Ind. – Arsenic-contaminated soil and groundwater pose risks to millions of Americans and hundreds of millions of people worldwide. Cleaning up the toxic metal is a laborious and expensive process, with some remediations of arsenic reaching into the hundreds of millions of dollars.
A fern – Pteris vittata, also known as the Chinese brake fern – holds promise for reducing both the time and cost associated with arsenic cleanup. It is unique because it can hyper-accumulate and tolerate very high levels of arsenic that it takes up from the soil, sequestering the toxic element in its fronds.
Scientists have now determined how this fern does it. Jody Banks, a Purdue professor of botany and plant pathology, and her team described the genetic and cellular mechanisms that control the fern’s arsenic tolerance in a paper published in the journal Current Biology. The findings could lead one day to the modification of other plants that would remediate arsenic from contaminated soils more quickly and efficiently.
“Other researchers have shown that this fern, when grown on arsenic-contaminated soils, can remove almost 50 percent of the arsenic in five years,” Banks said. “It takes time, but it’s cheap.”
Once inside cells - both human and plant – arsenic leads to cell death either through oxidative stress or by interfering with the cell’s ability to produce ATP, a molecule that provides energy for cells. But the fern has mechanisms that guard against these effects.
Banks and Chao Cai, a former graduate student in Banks’ lab, identified three genes that are highly active when the fern comes into contact with arsenic. Silencing each of these genes, they found, leads to death of the plant in the presence of arsenic, demonstrating their importance in arsenic tolerance. By testing the functions of the proteins encoded by these genes, they showed that these proteins may work together to essentially neutralize arsenic once inside the cell.
“These and other genes work together to mop up arsenic inside a cell until it can be stuffed safely away in the cell’s vacuole where it can’t do any harm,” Banks said.
The genes program three proteins – OCT4, GST and GAPC1. Banks and her team showed that OCT4 is a membrane protein, controlling the transfer of compounds through the cell membrane. GST is an arsenate reductase, which serves as a catalyst to turn arsenate from the soil into arsenite, the form of arsenic that can be sequestered.
The GAPC1 protein in other plants uses phosphate to help break down glucose for energy, and arsenate interferes with its normal function. In Pteris vittata fern, however, GAPC1 has a higher affinity for arsenate than phosphate, allowing the plant to tolerate the otherwise toxic substance.
Other researchers have discovered a bacterium, Pseudomonas aeruginosa, that has a similar ability to tolerate arsenic. The genetic mechanisms in the bacterium and the fern are nearly identical, suggesting that the fern evolved an arsenic tolerance mechanism that is similar to that used in bacterium.
“This fern has co-opted the same mechanism to tolerate arsenic that bacteria use,” Cai said. “And it is the only eukaryote that can do this. No plant or animal that we know of can do it like this fern.”
Understanding the genetic and cellular mechanisms that allow the fern to accumulate and tolerate arsenic is an important step in developing other plants that could remediate arsenic-contaminated soils and waters more quickly.
The National Science Foundation funded this research.
Writer: Brian Wallheimer, 765-532-0233, firstname.lastname@example.org
Source: Jody Banks, 765-494-5895, email@example.com
Three genes define a bacterial-like arsenic tolerance mechanism in the arsenic hyperaccumulating fern Pteris vittata
Chao Cai1, Nadia A. Lanman2, Kelley A. Withers3, Alyssa M. DeLeon1, Qiong Wu3, Michael Gribskov3, David E. Salt4 and Jo Ann Banks1
- Department of Botany and Plant Pathology, Purdue University, West Lafayette, IN
- Center for Cancer Research, Purdue University, West Lafayette, IN
- Department of Biological Sciences, Purdue University, West Lafayette, IN
- Division of Plant and Crop Sciences, School of Biosciences, University of Nottingham, UK
Arsenic is a carcinogenic contaminant of water and food and a growing threat to human health in many regions of the world. This study focuses on the fern Pteris vittata (Pteridaceae), which is extraordinary in its ability to tolerate and hyperaccumulate very high levels of arsenic that would kill any other plant or animal outside the Pteridaceae. Here we use RNA-seq to identify three genes (GLYCERALDEHYDE 3-PHOSPHATE DEHYDROGENASE (PvGAPC1), ORGANIC CATION TRANSPORTER 4 (PvOCT4) and GLUTATHIONE S-TRANSFERASE (PvGSTF1) that are highly up-regulated by arsenic and are necessary for arsenic tolerance, as demonstrated by RNAi. Our study reveals that the proteins encoded by these genes have unexpected properties: PvGAPC1 has an unusual active site and a much greater affinity for arsenate than phosphate (the substrate of GAPDH proteins); PvGSTF1 has arsenate reductase activity; and PvOCT4 (a membrane protein) localizes as puncta in the cytoplasm. Surprisingly, PvGAPC1, PvGSTF1 and arsenate also localize in a similar pattern. These results are consistent with a model that describes the fate of arsenate once it enters the cell. It involves the conversion of arsenate into 1-arseno-3-phosphoglycerate by PvGAPC1. This ‘chemically trapped’ arsenate is pumped into specific arsenic metabolizing vesicles by the PvOCT4 protein. Once inside these vesicles 1-arseno-3-phosphoglycerate hydrolyses rapidly to release arsenate, which is then chemically reduced by PvGSTF1 to arsenite, the form of arsenic stored in the vacuoles of this fern. This mechanism is strikingly similar to one recently described in the bacteria Pseudomonas aeruginosa whose tolerance to arsenic also involves the biosynthesis and transport of 1-arseno-3-phosphoglycerate, indicating that P. vittata has evolved a simple, bacterial-like mechanism for arsenic tolerance.
Agricultural Communications: 765-494-8415;
Maureen Manier, Department Head, firstname.lastname@example.org