| RESEARCH HIGHLIGHTS |
risk of developing the disease. Variations in this gene number could also predict whether IgAN patients would progress to end-stage kidney disease. The DEFA1A3 gene encodes an essential anti-microbial compound called α-defensin, which is released by immune cells during inflammatory responses. Liu and his colleagues replicated the analysis in a Caucasian population and found a similar
trend: fewer copies of the α-defensin gene in individuals with IgAN. Interestingly, however, the reduced occurrence of a four-nucleotide deletion observed in the Chinese IgAN group, which correlated with IgAN risk, was not seen in the Caucasian group. “We believe this locus con- tributes to the difference in prevalence between Caucasian and Chinese populations,” says Liu. “However, more studies of this locus, particularly
in the Caucasian population, will be needed to confirm and quantify this contribution.” The α-defensin protein expressed in this
region of the genome could offer potential targets for IgAN therapy, he adds.
1. Ai, Z., Li, M., Liu, W., Foo, J., Mansouri, O. et al. Low α-defensin gene copy number increases the risk for IgA nephropathy and renal dysfunction. Science Translational Medicine 8, 345ra88 (2016).
Molecular biology
VIRAL GATECRASHERS HAVE TRICK TO BOOST NUMBERS
A BLOCKING MECHANISM IS USED BY A MYSTERIOUS CLASS OF RETROVIRUSES TO FORCE THEIR HOST TO ALLOW THEM TO REPLICATE
Viruses hijack a body’s cellular machinery for their own reproduction. Scientists have shown how one class of virus uses a trick to override natural signals that would otherwise stop them from replicating. Researchers from the A*STAR Institute of
Molecular and Cell Biology have identified the mechanism through which one such virus — Moloney murine leukemia virus (MMLV) — is able to effectively ignore the RNA messages
This schematic illustrates how MMLV ignores 'stop signs' and facilitates syn- thesis of its proteins during replication.
Gag Inhibit termination eRF3 eRF1 UAG EPA 26 A*STAR RESEARCH EPA Promote readthrough EPA
known as stop-codons, which tell the body to stop translating genetic code into proteins. The project’s lead researcher, Haiwei Song,
explained that MMLV is one of a family of retroviruses, a type of virus that can insert itself into host DNA to replicate. “MMLV belongs to the gammaretro-
viruses, one genus of retroviruses recently implicated in human diseases,” he says. But the exact role of gammaretroviruses in causing
Gag pol RNase H
disease remains mysterious. In 2006, the gammaretrovirus XMRV
was identified in samples from men with prostate cancer. Some studies have found murine leukemia
virus (MLV), as well as XMRV, occurs at much higher rates in people with chronic fatigue syndrome than in healthy controls; however, others have not found this difference. “We don’t know the potential role of
XMRV and MLV in causing diseases such as prostate cancer and chronic fatigue syndrome, and the frequency of gammaret- rovirus infection among healthy people,” Song says. But a link common to all retroviruses is their ability to ignore RNA stop-codons. “Without this ability, the retroviruses will
simply not survive,” Song says. “So it is a very important target for antiviral intervention.” Identifying the mechanism gammaretrovi-
ruses use to ignore stop-codons could lead to new treatments, Song says.
ISSUE 6 | JANUARY – MARCH 2017
Reproduced from Ref. 1 and licensed under CC BY 4.0 (
https://creativecommons.org/licenses/by/4.0/) © 2016 X. Tang et al.
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56
