Changes between Version 229 and Version 230 of ChromosomeSegregation


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Timestamp:
Oct 23, 2015, 8:28:39 PM (5 years ago)
Author:
vw253
Comment:

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  • ChromosomeSegregation

    v229 v230  
    1414 ==  HIGHEST priority genes/complexes/papers ==
    1515
     16||Sid2||Chen et al. 2008||phosphorylates the nonessential Cdc14 phosphatase Clp1 to foster Clp1’s cytoplasmic retention||
    1617
    17 ||cdc2||PMID:8557037||mcs6 substrate cdc2 ||
    18 ||cdc2||PMID:6526270||uniprot has this paper for allele cdc2-4w C67F (we have 'unspecified')||
    19 ||Clp1||PMID:18378776 ||Clp1 in turn dephosphorylates the essential F-BAR scaffold protein Cdc15, CR assembly||
    20 ||plo1||?????||mid1? is a substrate||
    21 ||Sid2||Chen et al. 2008||phosphorylates the nonessential Cdc14 phosphatase Clp1 to foster Clp1’s cytoplasmic retention||
    22 ||Mre1 complex||PMID:21008122 and papers cited within|| In humans and both yeasts, DSBs are initially detected and processed by the 1Xrs2 (MRN) nucleolytic protein complex in association with the Tel1ATM checkpoint kinase and the Ctp1CtIP/Sae2 DNA-end processing factor;...implies tel1 /rad50/nbs1 should be annotated to GO:0000729 The functions of ATM and ATR orthologs are intimately tied to the detection and nucleolytic processing of DSBs. ATMTel1 localizes at DSBs by interacting with  (MRN) protein complex, which directly binds DNA ends (12, 20, 24, 50, 52).  use these papers to annotate the missing connection between tel1 and the mre11 complex ||
     18
     19
    2320||crb2||PMID:14739927 ||Finally, we show direct interaction between Rad3 and Crb2, which is inhibitory to Rad3 activity (direct enzyme regulator substrate) ||
    2421||crb2||PMID:21098122 ||There are two pathways that lead to Crb2 localization at sites of DNA damage (10). One pathway requires two inde- pendent histone modifications: (i) phosphorylation of the C- terminal tail of histone H2A ||
     
    2623|| crb2 ||????||Find physical interaction with Rad9||
    2724||All histones||????||These are often not annotated with their roles in cell cycle regulation and repair, and so they are excluded from the graphs (also need to have specific nucleosome terms, 'what do you call a normal nucleosome?l' and 'centromere specific'||
     25
    2826||srw1||PMID:9571240, PMID:9736616 PMID:10921878 ||has no mitotic cell cycle regulation annotation||
    2927|| fnx1 & 2||PMID: 18503766 || This wouldn't normally be a priority, but I'm putting it in becasue the exisitng transport GO annotations look a bit of a mess (stretch) ... need to get detailed phenotypes and then decide what it is possible to infer sensibly||
     
    3230||dsc2||???||activation of sre2 TF? positive regulation of SREBP signaling pathway by transcription factor cleavage? for the Dsc subunits? may be in one of the other dsc papers.... chung paper?||
    3331||cul1||?????||-||
    34 ||ppa1||?????||targets ppe1?||
    35 ||ppe1||?????||targets pim1?||
    36 ||pck1||?????||targets ppe1?||
    3732||pck1||?????||phosphorylates  mcm2,4,6, caf1, swi6,rad9, swi3, mrc1 crm1 and other importins||
    3833||Pad1/Rpn11 and Mts3/Rpn12 are subunits of the lid subcomplex||?????|| in PMID: 16149916 Mutations in the genes encoding these two subunits were isolated in a screen for mutants that were both esistant to methyl 2-benzimidazolecarbamate, a microtubule in- hibitor, and Ts for cell-cycle progression [19,20]. Ts mutations in both genes cause arrest of the cells in mitosis, probably because of a failure to degrade cyclin B/Cdc13 and securin/Cut2. ||
    3934|| mde4 ||?????|| Previous results showed that in interphase, when Mde4 is dephosphorylated, the Mde4-Pcs1 complex localizes to the nucleolus and to the kinetochores, which cluster at the nuclear periphery next to the spindle pole bodies (SPBs) [6,8]. As cells enter mitosis and Mde4 becomes phosphorylated, Mde4- Pcs1 leave the nucleolus but remain at the kinetochores [6,8]. PubMed: 17627824/12689592]||
    4035||cdc20|| ?????|| When Cdc20 is overexpressed, securin can be degraded during interphase, whereas other destruction box proteins will remain stable. In cells lacking Cdc20, securin remains stable, and sister chromatids will not separate (Visintin et al., 1997).||
    41 ||cut7|||?????|| In the temperature-sensitive cut7 mutant, spindle formation is blocked shortly after duplication of the SPB. The mitotic spindle radiating from the opposite poles cannot interdigitate and thus remains as a V shape (Hagan and Yanagida, 1992). The cut7- specific defect generates a condition whereby the bipolar attachment of the spindle to kinetochores is not achieved. Previously, we demonstrated that this defect causes an arrest in a mad2+-dependent manner (Kim et al., 1998). At the restrictive temperature the majority of Mad2-GFP was found on condensed chromosomes as one or more speckles (Fig. 4).||
     36
    4237|| fin1|| PMID:23333317 PMID:22684255 ||priority papers for G2/M network||
    43 || nif1|| ??? ||priority papers for G2/M network, need interactors, targets||
    44 ||TOR pathway||priority papers for G2/M network, need interactors, targets||
    45 ||skb1||PMID: 23615447 ||priority papers for G2/M network, need interactors, targets||
    4638||plo1||??? ||priority papers for G2/M network, need to annotate papers which capture plo1 role in mitotic G2/M transition AND cdc25 target, and plo1 as a target of MAPK signalling||
    4739
     
    117109||mad2 & SCC ||mad2 targets slp1 acting as a mitotic anaphase-promoting complex inhibitor activity||---||
    118110
     111===
    119112||dis1 ||PMID:16920624 plus…XMAP215/ TOG/Stu2-family homolog, binds microtubules and localizes to kinetochores (Nakaseko et al., 2001). Mutants in dis1 lack the chromosome alignment phase in metaphase and arrest with elongated spindles and segregated but unseparated chromosome pairs (Nabe- shima et al., 1998; Ohkura et al., 1988).dis1 mutants arrest with an activated spindle checkpoint and appear to ex- perience an increase in sister chromatid cosegregation (70%) at full restrictive temperature. Such cosegregation results when mono-oriented attachment of sister kineto- chores to microtubules from the same SPB is not corrected. Since dis1 mutants lack the phase of constant spindle length when chromosomes are properly aligned ||-||
    120113|| dis2 phosphatase  ||  (PMID:14765108 - describes checkpoint termination Dis2 abrogates Chk1 phosphorylation and activation in vivo, ) PMID:2245912   PMID:8389306 PMID:8305731 PMID:7983142 PMID:7957097 PMID:9264466 PMID:9790575 PMID:10668632 PMID:11085271 PMID:16411888 PMID:17895368 PMID:19592249 PMID:21664573 (Out for CC PMID:21703453 PMID:21965289 PMID:23333317)  (Iain Hagan  PMID:25487150) || -||
     114||cut7|||?????|| In the temperature-sensitive cut7 mutant, spindle formation is blocked shortly after duplication of the SPB. The mitotic spindle radiating from the opposite poles cannot interdigitate and thus remains as a V shape (Hagan and Yanagida, 1992). The cut7- specific defect generates a condition whereby the bipolar attachment of the spindle to kinetochores is not achieved. Previously, we demonstrated that this defect causes an arrest in a mad2+-dependent manner (Kim et al., 1998). At the restrictive temperature the majority of Mad2-GFP was found on condensed chromosomes as one or more speckles (Fig. 4).||
    121115
    122116 === Notes and annotation questions on chromosome segregation ===