MadR1, a Mycobacterium tuberculosis cell cycle stress response protein that is a member of a widely conserved protein class of prokaryotic, eukaryotic and archeal origin.
MadR1, a Mycobacterium tuberculosis cell cycle stress response protein that is a member of a widely conserved protein class of prokaryotic, eukaryotic and archeal origin.
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MADR1,一种结核分枝杆菌细胞周期应力反应蛋白,是广泛保守的原核生物,真核和弓形的蛋白质类别的成员。
DOI:
10.1016/j.tube.2015.03.005
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发表时间:
2015-05
期刊:
影响因子:
--
通讯作者:
Slayden RA
中科院分区:
文献类型:
--
作者:
Crew R;Ramirez MV;England K;Slayden RA
Stress-induced molecular programs designed to stall division progression are nearly ubiquitous in bacteria, with one well-known example being the participation of the SulA septum inhibiting protein in the SOS DNA damage repair response. Mycobacteria similarly demonstrate stress-altered growth kinetics, however no such regulators have been found in these organisms. We therefore set out to identify SulA-like regulatory proteins in Mycobacterium tuberculosis. A bioinformatics modeling-based approach led to the identification of rv2216 as encoding for a protein with weak similarity to SulA, further analysis distinguished this protein as belonging to a group of previously uncharacterized growth promoting proteins. We have named the mycobacterial protein encoded by rv2216 morphology altering division regulator protein 1, MadR1. Overexpression of madR1 modulated cell length while maintaining growth kinetics similar to wild-type, and increased the proportion of bent or V-form cells in the population. The presence of MadR1-GFP at regions of cellular elongation (poles) and morphological differentiation (V-form) suggests MadR1 involvement in phenotypic herterogeneity and longitudinal cellular growth. Global transcriptional analysis indicated that MadR1 functionality is linked to lipid editing programs required for growth and persistence. This is the first report to differentiate the larger class of these conserved proteins from SulA proteins and characterizes MadR1 effects on the mycobacterial cell.
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影响因子:
2.8
作者:
Dullaghan, EM;Brooks, PC;Davis, EO
通讯作者:
Davis, EO
影响因子:
3.2
作者:
MAGUIN, E;LUTKENHAUS, J;DARI, R
通讯作者:
DARI, R
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3.2
作者:
Au, N;Kuester-Schoeck, E;Lovett, CM
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Lovett, CM
影响因子:
14.9
作者:
Altenhoff AM;Schneider A;Gonnet GH;Dessimoz C
通讯作者:
Dessimoz C
影响因子:
3.2
作者:
Gallwitz, Maike;Reimer, Jenny M.;Hellman, Lars
通讯作者:
Hellman, Lars