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. 2015 Oct 12;16:769. doi: 10.1186/s12864-015-1979-1

Table 1.

Summary of 25 genes producing RNAi phenotypes

Gene E–value KOG group Functional category Phenotype
Smed–slbp 1.00E–10 Histone mRNA stem–loop binding protein [A] RNA processing and modification Loss of stem cells
Smed–sart3 4.00E–102 RNA–binding protein SART3 [A] RNA processing and modification Loss of stem cells
Smed–smarcc–1 2.00E–08 Chromatin remodeling factor subunit and related transcription factors [B] Chromatin structure and dynamics Loss of stem cells
Smed–cycD 2.00E–10 G1/S–specific cyclin D [D] Cell cycle control, cell division, chromosome partitioning Loss of stem cells
Smed–espl1 3.00E–32 Regulator of spindle pole body duplication [D] Cell cycle control, cell division, chromosome partitioning Loss of stem cells
Smed–rrm2b–1 6.00E–28 Ribonucleotide reductase, beta subunit [F] Nucleotide transport and metabolism Loss of stem cells
Smed–rrm2b–2 3.00E–143 Ribonucleotide reductase, beta subunit [F] Nucleotide transport and metabolism Loss of stem cells*
Smed–pdss2/dlp1 1.00E–28 Geranylgeranyl pyrophosphate synthase/ Polyprenyl synthetase [H] Coenzyme transport and metabolism Loss of stem cells*
Smed–dkc1 5.00E–149 Pseudouridine synthase [J] Translation, ribosomal structure and biogenesis Loss of stem cells
Smed–emg1/nep1 1.00E–26 Protein required for 18S rRNA maturation and 40S ribosome biogenesis [J] Translation, ribosomal structure and biogenesis Loss of stem cells*
Smed–lig1 9.00E–125 ATP–dependent DNA ligase I [L] Replication, recombination and repair Loss of stem cells
Smed–prim2 1.00E–99 Eukaryotic–type DNA primase, large subunit [L] Replication, recombination and repair Loss of stem cells
Smed–mcm7 0 DNA replication licensing factor, MCM7 component [L] Replication, recombination and repair Loss of stem cells*
PL08006B2E08 –– No significant homology none Loss of stem cells
Smed–rbap46/48–2 3.00E–79 Nucleosome remodeling factor, subunit CAF1/NURF55/MSI1 [B] Chromatin structure and dynamics Six feedings – reduced/delayed regeneration, reduced mitosis Three feedings – elongated photoreceptor pigment
Smed–mcm2 2.00E–148 DNA replication licensing factor, MCM2 component [L] Replication, recombination and repair Reduced/delayed regeneration, asymmetric photoreceptors, reduced mitosis
Smed–ptbp1 2.00E–54 Polypyrimidine tract–binding protein [A] RNA processing and modification Reduced/delayed regeneration, forked tail, inching movement, lysis
Smed–fen–1 1.00E–149 5′–3′ exonuclease [L] Replication, recombination and repair Reduced/delayed regeneration
Smed–morf4l1/mrg–1 5E–26 Dosage compensation regulatory complex/ histone acetyltransferase complex, subunit MSL–3/MRG15/EAF3 [BK] Chromatin structure and dynamics, transcription Reduced/delayed regeneration, lysis
Smed–ddc 2.00E–57 Aromatic–L–amino–acid/L–histidine decarboxylase [E] Amino acid transport and metabolism Faint photoreceptor pigment
Smed–tph 0 Aromatic amino acid hydroxylase [E] Amino acid transport and metabolism No photoreceptor pigment, elongated, inching movement
Smed–gas8 9.00E–87 No significant homology None Edema
Smed–pgbd4 1.00E–05 No significant homology None Lesion at posterior of pharynx, dorsal hump, bulged sides, loss of pharynx, impaired photoreceptor development
Smed–b9d2 9.00E–75 Uncharacterized conserved protein [S] Function unknown Inching movement
Smed–ima–1 1.00E–104 Karyopherin (importin) alpha [U] Intracellular trafficking, secretion, and vesicular transport Collapse toward midline, cyclops/asymmetric photoreceptors, reduced mitosis

Only genes producing a phenotype are shown; see Additional file 4 for a full list of genes tested. Gene names were assigned based on homology from BLASTx searches against the NCBI database. E–values are the lower value between BLASTx of the cloned EST or a longer sequence from published transcriptomes [13, 14] against the corresponding human protein. KOG group and functional category assignments were made using the eukaryotic Clusters of Orthologous Groups database [49]. An asterisk (*) indicates that loss of stem cells was verified by staining with anti–phospho–Histone H3