TY - JOUR
T1 - Identification of an Alternating-Access Dynamics Mutant of EmrE with Impaired Transport
AU - Wu, Chao
AU - Wynne, Samantha A.
AU - Thomas, Nathan E.
AU - Uhlemann, Eva Maria
AU - Tate, Christopher G.
AU - Henzler-Wildman, Katherine A.
N1 - Funding Information:
This work was funded by grants from NIH R01GM095839 to KHW and core funding from the Medical Research Council [MRC U105197215 ] to CGT. NET was supported by NIH National Research Service Award T32 GM007215 . NMR data were collected both at Washington University in St. Louis and at the National Magnetic Resonance Facility at Madison. NMRFAM is supported by NIH grant P41GM103399 (NIGMS), old number: P41RR002301 . Equipment was purchased with funds from the University of Wisconsin–Madison, the NIH ( P41GM103399 , S10RR02781 , S10RR08438 , S10RR023438 , S10RR025062 , S10RR029220 ), the NSF ( DMB-8415048 , OIA-9977486 , BIR-9214394 ), and the USDA. We thank Changguo Tang and Greg DeKoster at Washington University in St. Louis and Marco Tonelli at NMRFAM for assistance in implementing NMR pulse sequences. Some of the ITC replicates were obtained at the University of Wisconsin–Madison Biophysics Instrumentation Facility, which was established with support from the University of Wisconsin–Madison and grants BIR-9512577 (NSF) and S10RR13790 (NIH).
Funding Information:
This work was funded by grants from NIH R01GM095839 to KHW and core funding from the Medical Research Council [MRC U105197215] to CGT. NET was supported by NIH National Research Service Award T32 GM007215. NMR data were collected both at Washington University in St. Louis and at the National Magnetic Resonance Facility at Madison. NMRFAM is supported by NIH grant P41GM103399 (NIGMS), old number: P41RR002301. Equipment was purchased with funds from the University of Wisconsin–Madison, the NIH (P41GM103399, S10RR02781, S10RR08438, S10RR023438, S10RR025062, S10RR029220), the NSF (DMB-8415048, OIA-9977486, BIR-9214394), and the USDA. We thank Changguo Tang and Greg DeKoster at Washington University in St. Louis and Marco Tonelli at NMRFAM for assistance in implementing NMR pulse sequences. Some of the ITC replicates were obtained at the University of Wisconsin–Madison Biophysics Instrumentation Facility, which was established with support from the University of Wisconsin–Madison and grants BIR-9512577 (NSF) and S10RR13790 (NIH).
Funding Information:
This work was funded by grants from NIH R01GM095839 to KHW and core funding from the Medical Research Council [MRC U105197215] to CGT. NET was supported by NIH National Research Service Award T32 GM007215. NMR data were collected both at Washington University in St. Louis and at the National Magnetic Resonance Facility at Madison. NMRFAM is supported by NIH grant P41GM103399 (NIGMS), old number: P41RR002301. Equipment was purchased with funds from the University of Wisconsin?Madison, the NIH (P41GM103399, S10RR02781, S10RR08438, S10RR023438, S10RR025062, S10RR029220), the NSF (DMB-8415048, OIA-9977486, BIR-9214394), and the USDA. We thank Changguo Tang and Greg DeKoster at Washington University in St. Louis and Marco Tonelli at NMRFAM for assistance in implementing NMR pulse sequences. Some of the ITC replicates were obtained at the University of Wisconsin?Madison Biophysics Instrumentation Facility, which was established with support from the University of Wisconsin?Madison and grants BIR-9512577 (NSF) and S10RR13790 (NIH).
Publisher Copyright:
© 2019 The Authors
PY - 2019/7/12
Y1 - 2019/7/12
N2 - Proteins that perform active transport must alternate the access of a binding site, first to one side of a membrane and then to the other, resulting in the transport of bound substrates across the membrane. To better understand this process, we sought to identify mutants of the small multidrug resistance transporter EmrE with reduced rates of alternating access. We performed extensive scanning mutagenesis by changing every amino acid residue to Val, Ala, or Gly, and then screening the drug resistance phenotypes of the resulting mutants. We identified EmrE mutants that had impaired transport activity but retained the ability to bind substrate and further tested their alternating access rates using NMR. Ultimately, we were able to identify a single mutation, S64V, which significantly reduced the rate of alternating access but did not impair substrate binding. Six other transport-impaired mutants did not have reduced alternating access rates, highlighting the importance of other aspects of the transport cycle to achieve drug resistance activity in vivo. To better understand the transport cycle of EmrE, efforts are now underway to determine a high-resolution structure using the S64V mutant identified here.
AB - Proteins that perform active transport must alternate the access of a binding site, first to one side of a membrane and then to the other, resulting in the transport of bound substrates across the membrane. To better understand this process, we sought to identify mutants of the small multidrug resistance transporter EmrE with reduced rates of alternating access. We performed extensive scanning mutagenesis by changing every amino acid residue to Val, Ala, or Gly, and then screening the drug resistance phenotypes of the resulting mutants. We identified EmrE mutants that had impaired transport activity but retained the ability to bind substrate and further tested their alternating access rates using NMR. Ultimately, we were able to identify a single mutation, S64V, which significantly reduced the rate of alternating access but did not impair substrate binding. Six other transport-impaired mutants did not have reduced alternating access rates, highlighting the importance of other aspects of the transport cycle to achieve drug resistance activity in vivo. To better understand the transport cycle of EmrE, efforts are now underway to determine a high-resolution structure using the S64V mutant identified here.
KW - NMR
KW - Transport
KW - alternating-access
KW - dynamics
KW - structure
UR - http://www.scopus.com/inward/record.url?scp=85066924539&partnerID=8YFLogxK
U2 - 10.1016/j.jmb.2019.05.035
DO - 10.1016/j.jmb.2019.05.035
M3 - Article
C2 - 31158365
AN - SCOPUS:85066924539
VL - 431
SP - 2777
EP - 2789
JO - Journal of Molecular Biology
JF - Journal of Molecular Biology
SN - 0022-2836
IS - 15
ER -