the truth is that most medical breakthroughs have ultimately come from basic research , and i think that we as scientists need to do a better job of telling these success stories . my favorite example is that antibiotics came out of finding a random contaminant on a plate . and remember that we have crispr [ clustered regularly interspaced short palindromic repeats ] tools only because people were studying some bizarro antipathogen mechanism in bacteria . it s a beautiful example of something entirely unanticipated coming out of left field . that s why it s important to maintain funding for a very diverse program of basic research ; history tells us you ca nt predict where the next advance will come from . right now it seems like funding agencies and the public have an engineering mentality , and they believe that , as long as we think hard enough about a problem , we can solve it . that s an admirable attitude , but in the life sciences it s not always the right path to discovery . i would argue that under some circumstances , studying yeast cells is a better idea than studying highly transformed human cells in a dish . for many years , we used to write in the  significance  section of grant applications that the reason that it is important to understand chromosome segregation is because , when it fails , cells become aneuploid and cancerous . why should aneuploidy cause cells to proliferate ? when you do yeast crosses and by chance get an aneuploid strain , invariably the cells do poorly . and one explanation is that building an organism is a complicated procedure , so if you change the gene dosage of certain genes , you mess everything up . that s probably true you could then further argue that , at the cellular level , maybe it does nt really matter how many chromosomes you have , as long as you have at least one of each . perhaps extra chromosomes are actually good for an individual cell and allow it to keep proliferating when they should not and this gives you cancer . however , we never thought this was very likely , given that aneuploid yeast often proliferate poorly . you can very agnostically ask : what happens to a cell if you change the chromosome number ? yeast was the right organism for this because we have genetic tricks and selection methods to generate aneuploids that are stable enough to study . because this allowed us to examine many different types of aneuploidies at the same time , we could look for broad patterns . we could nt have done it in any other organism . actually , we do all our discovery work in yeast . and when we find something interesting , we move it into the mouse or human cell lines and ask whether we see the same thing . sometimes the answer is  no ,  but more often the answer is  yes . it s just harder to discover fundamentally new things in very complex organisms where the repertoire of tools is limited . and i would argue that , under some circumstances , studying yeast cells is a better idea than studying highly transformed human cells in a dish . angelika amon s work over the past 15 years has guided all of us who think about mitotic and meiotic cell division . , we wondered whether there was a systematic way the cell avoids losing or gaining chromosomes . to be honest , i was hoping there would be some kind of cute mechanism that counts chromosomes . that turned out to be completely wrong . or at least we havent been able to find anything of this sort . once we realized that , we had to step back and let the genetics lead the way . we did a lot of phenotypic characterization and then developed hypotheses to explain the patterns we saw . if complex subunits are not expressed in the correct ratios , often unassembled subunits need chaperones to maintain their soluble state and eventually need to be degraded if they can not find a binding partner . cancer cells do nt only lose or gain whole chromosomes , they also have translocations and deletions and point mutations . we know that making and repairing dna requires a lot of nifty multi - subunit complexes , so our hypothesis was that whole - chromosome abnormalities cause stoichiometric imbalances in these complexes and this leads to defects in their formation and function . so we re testing the idea that aneuploidy contributes to cancer because it s a mutator , rather than because it s a promoter of growth and proliferation , and we re doing more and more mouse work to answer those kinds of questions . but we still use yeast to discover new properties of aneuploidy and to look at the cellular effects of changing the dosage of specific genes . we started a new project on mitochondria a few years ago that i m really excited about . one big question is : how did these two organisms start talking to each other ? did one learn english or the other learn french ? or did they resort to a more primitive sign language  metabolites  to talk to each other ? the other thing i m fascinated by is that a large fraction of uncharacterized yeast genes localize to mitochondria . that tells you there s a lot of biology in the mitochondria still to be learned . what i think is even more important is that many of these genes are not at all conserved , not even in fungi . so here are all these very new , very fast - evolving genes and nobody knows what they do ! usually when people hear that a gene is not conserved , they run !  arrgh ! it s something yeast specific !  but in this particular instance i think it s important and suggests mitochondria are still battling it out with the nucleus . one way to look at it is to say the nucleus and mitochondria are not really symbiotic . if mitochondria do nt get anything out of the relationship , they are really just slaves to the nucleus . so the mitochondria are trying to escape the reign of the nucleus and the nucleus is fighting back in an arms race . and if we can understand what all these nonconserved mitochondrial genes are doing , we can begin to find the frictions that still exist between the interests of the nucleus and the mitochondria . i m totally fascinated by understanding how these different entities interact with each other inside a single cell .
the genetics society of america medal is awarded to an individual for outstanding contributions to the field of genetics in the past 15 years . 
 recipients of the gsa medal are recognized for elegant and highly meaningful contributions to modern genetics . 
 the 2014 recipient , angelika b. amon , has uncovered key principles governing the cell cycle and was the first to demonstrate a connection between the physical completion of anaphase and the initiation of mitotic exit . 
 more recently , her research has focused on the consequences of aneuploidy . 
 genetics spoke with dr . 
 amon about her approach to science and what is next on the horizon .