Deletion of POM34 or POM152 disrupted the function of essential SPB duplication regulator, Mps2. These data, combined with our data on Ncs2, Nup60, and Pom152, further implicate the nuclear pore in proper assembly of the SPB and suggest that the urmylation pathway may act in conjunction with nuclear pore components to regulate SPB size. Our screen also identified Ubc4, the ubiquitin-conjugating enzyme. In mammalian cells, tumor suppressor BRCA1 uses a Ubc4 homolog as one of its ubiquitin E2 ligases for conjugating ubiquitin to target proteins. It has also been shown that BRCA1-dependent ubiquitination is important in regulating centrosome number, and centrosome amplification is a hallmark of cancer. Our results show that Ubc4 but not its close relative, Ubc5, regulates the size of SPBs during asynchronous growth. Deletion of UBC4 leads to disruption of SPB size regulation as indicated by increased levels of Spc110 and Spc42 in the poles. Ubiquitination of target proteins by Ubc4 could regulate SPB size by altering levels of SPB proteins or by affecting their incorporation into the pole, thereby changing the nucleation capacity of the SPB. BRCA1 regulates centrosome nucleation activity through ubiquitination of c-tubulin and a centrosome adaptor component, and our data implicate Ubc4 in a conserved centrosome regulation pathway in yeast. Malaria is a mosquito-borne disease and remains a major BI-D1870 global health problem causing illness and death that disproportionately affects developing countries. The worldwide incidence of malaria is estimated by the Word Health Organization to be approximately 300 to 500 million clinical cases annually, with one million deaths, the majority of which are young children. Of particular concern, the emergence of insecticide-resistant mosquito vectors and multi-drug resistant parasites has contributed to resurgences of the disease. Therefore, malaria control is a continuous battle that requires long-term sustainability and commitment. The development of a vaccine that reduces morbidity and mortality would be a valuable new tool in the fight against malaria. Plasmodium falciparum causes the most severe form of the disease. Infection begins when malaria sporozoites are injected by mosquito into the host and within minutes parasites invade hepatocytes, where they multiply and differentiate into the next stage. The emerging merozoites invade red blood cells leading to clinical illness. The most advanced vaccine candidate, designated RTS,S/AS02A, is based on the major sporozoite surface antigen. However, this candidate vaccine, currently in Phase 3 clinical trials, has shown only 30–65% efficiency in field studies and a vaccine with higher levels of protection is still sought. Over time, people living in malariaendemic areas develop immunity to clinical disease caused by P. falciparum and IgG from immune adults has been shown to reduce parasite density and clinical symptoms when administered to children with clinical malaria.