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. 2019 Jan 10;213(4):1145–1188. doi: 10.1534/genetics.119.300238

Table 3. Genes that promote meiotic development—enhancer of weak glp-1 gain of function.

Genea Product Human homolog Evidenceb Reference(s)
Pre-mRNA splicing
 mog-1 Yeast PRP16 related splicing factor DHX38 2,4 Belfiore et al. (2004); Kerins et al. (2010)
 mog-4 Yeast PRP2 related splicing factor DHX16 2 Belfiore et al. (2004); Kerins et al. (2010)
 mog-5 Yeast PRP22 related splicing factor DHX8 2 Belfiore et al. (2004); Kerins et al. (2010)
 cyn-4 cyclophilin peptidylprolyl PPIL2 2,4 Belfiore et al. (2004); Kerins et al. (2010)
 (aka mog-6) Isomerases
 prp-17 Yeast PRP17 related splicing factor CDC40 2,4 Kerins et al. (2010)
 prp-19 Yeast PRP19 related splicing factor PRPF19 1 Gutnik et al. (2018)
 teg-1 CD2 cytoplasmic tail-binding protein CD2BP2 2,4 Wang et al. (2012)
 teg-4 Splicing factor 3b subunit 3 SF3B3 2,4 Mantina et al. (2009)
Ubiquitin-mediated proteolysis
 pas-5 20S proteasome alpha-type five subunit PSMA5 2,4 Macdonald et al. (2008)
 sel-10 SCF E3 ubiquitin ligase FBXW7 1,6 Pepper et al. (2003a)
 sel-11 E3 ubiquitin ligase SYVN1 1,6 Choi et al. (2010)
 rfp-1 E3 ubiquitin ligase RNF40 3 Gupta et al. (2015)
 ubr-5 E3 ubiquitin ligase UBR5 1,6 Safdar et al. (2016)
RNA N6-adenosine methyltransferase
 mett-10 Methyltransferase 10 domain containing METTL16 1,2,5 Dorsett et al. (2009)
Miscellaneous
 puf-8 Pumilio RNA-binding family member PUM1/PUM2 1 Racher and Hansen (2012)
 kin-10 Casein kinase 2 beta CSNK2B 2,4 Wang et al. (2014)
 him-17 THAP domain containing 3 Bessler et al. (2007)
a

For all genes listed, RNAi or double mutant with weak glp-1(gf) at the permissive temperature results in a strong overproliferation phenotype.

b

For a gene to be included in the table, at least one additional line of experimentation (evidence 1–6, below) must be available that informs on its function in the stem cell vs. meiotic development decision. 1, RNAi or double mutant results partial or complete suppression of a glp-1(rf) at the restrictive temperature; 2, RNAi or double mutant results in a synthetic tumorous phenotype with gld-2 null and/or with gld-3 null; 3, RNAi or double mutant does not result in a synthetic tumorous phenotype with gld-2 null and/or with gld-3 null; 4, RNAi or triple mutant results in a synthetic tumorous phenotype with gld-3 null and glp-1 null; 5, RNAi or triple mutant results in a Glp-1 like phenotype with gld-3 null and glp-1 null; 6, RNAi or mutant suppresses weak lin-12 loss of function.