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SUMMARY:Checkpoint and non-checkpoint functions of Drosophila Mad1 and RZZ
 .  - Professor Roger Karess\, Institut Jacques Monod\, Université Paris D
 iderot
DTSTART:20160211T140000Z
DTEND:20160211T150000Z
UID:TALK60487@talks.cam.ac.uk
CONTACT:Caroline Newnham
DESCRIPTION:My group has been studying the regulation of mitosis by the Sp
 indle Assembly Checkpoint (SAC)\, by exploiting the genetics and cell biol
 ogy of Drosophila.  We have recently been focusing on two components of th
 e SAC\,  Mad1 and RZZ.  Proper recruitment of Mad1 to unattached kinetocho
 res requires the RZZ complex\, by a mechanism that remains to be elucidate
 d.  \n\nThe more we study these proteins\, the more surprises they offer u
 p. My talk will have two parts. First I will describe an interesting point
  mutation in the RZZ subunit Rod that appears to block RZZ and Mad1 recrui
 tment in early syncytial embryos but not later in development\, suggesting
  that kinetochores may possess some stage- or tissue-specific properties. 
  I will then focus on Mad1 and the evidence we have accumulated that this 
 classical spindle checkpoint protein has an additional role in interphase 
 nuclei quite unrelated to mitosis.  Mad1\, unlike Mad2\, is present in all
  nuclei of Drosophila\, including postmitotic tissues.  Mad1 associates wi
 th a set of proteins potentially involved in chromatin organization. These
  proteins colocalize with Mad1 in Intranuclear Territories (“MINTs” ) 
 In spermatocytes\, where chromatin is structured into three well-spaced ma
 sses\, one can see these MINTs particularly clearly.  Removal of Mad1 affe
 cts both the intranuclear localization of these partner proteins and chrom
 atin packaging.  The mitotic phenotype of a mad1 null may therefore reflec
 t not just a defective spindle checkpoint but also consequences of aberran
 t interphase chromatin organization.  
LOCATION:Biffen Lecture Theatre\, Department of Genetics\, Downing Site
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