increased chromatin silencing

[ValWood]

Check. Silencing is the default for centromere, some of these seem to be "increase in the extent of chromatin silencing"

increased chromatin silencing at centromere

• [ ]  cut8 (1-72) (73-262 Δaa)[Overexpression],    (move to central core)

• [ ] rpt3-1 (Q384->stop)[Wild type product level] (move to central core)

• [ ] SPAC18B11.07c | rhp6 | Rad6 homolog, ubiquitin conjugating enzyme E2 Rhp6

• [ ] SPCC1682.16 | rpt4 | 19S proteasome base subcomplex ATPase subunit Rpt4

• [ ] SPBC1105.09 | ubc15 | ubiquitin conjugating enzyme E2 Ubc15

• increased chromatin silencing at centromere inner repeat

• [ ] hos2Δ

• increased chromatin silencing at centromere otr1L

• [x] | epe1Δ,  

• [x]  leo1:Hermes (disruption)

  increased chromatin silencing at centromere outer repeat

• [ ] eri1-AA (H264A, D268A aa),   eri1Δ

• [ ] SPAC664.03 | paf1 | RNA polymerase II associated Paf1 complex (predicted)

• [ ] SPAC664.01c | swi6 | heterochromatin (HP1) family chromodomain protein Swi6

also some of the non-MT,CEN,telomere locations may be increased silencing but in euchromatin not heterochromatin

[ValWood]

PMID:26518661

Mating type region Given the role of Leo1 in Paf1C, we compared the effects on IR‐L silencing following the deletion of genes encoding the other components of the protein complex. In addition to leo1∆, paf1∆ enhanced silencing within IR‐L and extended the silent domain into the matL region. However, deletion of tpr1 + or cdc73 + had little or no effect on chromatin silencing (Fig 2B). These observations demonstrate that the Leo1–Paf1 heterodimer rather than the complete Paf1C prevents the propagation of the repressed state across the IR‐L boundary element.

centromeric

This is a red flag odd because the annotations are

leo1 | leo1:Hermes(disruption)[Not assayed] | FYPO:0006992 | normal chromatin silencing at centromere otr1R | Chromatin immunoprecipitation experiment

leo1 | leo1:Hermes(disruption)[Not assayed] | FYPO:0006994 | increased chromatin silencing at centromere otr1L | Chromatin immunoprecipitation experiment |

This should be a red flag because there should be no difference between Left and right. Anyway this is about heterochromatin spreading beyond the normal otrL boundary element

By combining the reporter gene ura4 + integrated at different positions in the left pericentric region of centromere 1 with leo1 mutations, we demonstrated that the heterochromatin defects observed in the RNAi‐deficient mutants were rescued by the leo1::Hermes allele as heterochromatin was restored (Fig 5C).

so really this isn't assaying a phenotype against WT, it's a rescue experiment with silencing mutants

[ValWood]

Got it To identify factors required for heterochromatin boundary maintenance in S. pombe, we applied a random mutagenesis assay and screened the resulting mutants for the silenced reporter genes ade6 + and ura4 +, which were integrated at regions of normally open chromatin. The ade6 + reporter gene was positioned at the inverted repeat boundary to the left (IR‐L) of the silent matK region, whereas the ura4 + gene was integrated 1.2 kb further into the euchromatic matL region (Fig 1A). The cells show no phenotype when grown on complete media (YEA or YES) under non‐selective conditions. However, the cells will be resistant to 5‐fluorotic acid (5FOA) when ura4 + is silenced 36

SO the assy isn't assaying in the normally heterochromatin region of ILR , it's assaying just outside it (TO THE LEFT OF ILR). So, in some cases an increase of silencing is observed. I will request a new term for this.

[ValWood]

PMID:24710126 refer to central core "A previous study31 showed that silencing of the ura4+ gene inserted at cnt1 is moderate and allows growth on 5-fluoroorotic acid (FOA) at 26 °C in a wild-type background." so silencing at the central core can increase....