scholarly journals Sampling and analysis of the inactive waste tanks TH-2, WC-1, and WC-15. Environmental Restoration Program

1992 ◽  
Author(s):  
J.W. Autrey ◽  
J.M. Keller ◽  
W.H. Griest ◽  
J.L. Botts ◽  
R.L. Schenley ◽  
...  
Keyword(s):  
Environmental Restoration ◽  
Waste Tanks

scholarly journals Correction to “Identification of the Non-Pertechnetate Species in Hanford Waste Tanks, Tc(I)–Carbonyl Complexes”

2021 ◽  
Vol 55 (4) ◽  
pp. 2705-2705
Author(s):  
Wayne W. Lukens ◽  
David K. Shuh ◽  
Norman C. Schroeder ◽  
Kenneth R. Ashley
Keyword(s):  
Carbonyl Complexes ◽  
Waste Tanks

scholarly journals Germ granule dysfunction is a hallmark and mirror of Piwi mutant sterility

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Maya Spichal ◽  
Bree Heestand ◽  
Katherine Kretovich Billmyre ◽  
Stephen Frenk ◽  
Craig C. Mello ◽  
...  
Keyword(s):  
Dna Damage ◽  
Genomic Instability ◽  
Environmental Restoration ◽  
Related Gene ◽  
C Elegans ◽  
Dna Damage Signaling ◽  
Multiple Phenotypes ◽  
Granule Structure ◽  
Germ Granules ◽  
Late Generation

AbstractIn several species, Piwi/piRNA genome silencing defects cause immediate sterility that correlates with transposon expression and transposon-induced genomic instability. In C. elegans, mutations in the Piwi-related gene (prg-1) and other piRNA deficient mutants cause a transgenerational decline in fertility over a period of several generations. Here we show that the sterility of late generation piRNA mutants correlates poorly with increases in DNA damage signaling. Instead, sterile individuals consistently exhibit altered perinuclear germ granules. We show that disruption of germ granules does not activate transposon expression but induces multiple phenotypes found in sterile prg-1 pathway mutants. Furthermore, loss of the germ granule component pgl-1 enhances prg-1 mutant infertility. Environmental restoration of germ granule function for sterile pgl-1 mutants restores their fertility. We propose that Piwi mutant sterility is a reproductive arrest phenotype that is characterized by perturbed germ granule structure and is phenocopied by germ granule dysfunction, independent of genomic instability.

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