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Research in the Singson lab

Fertilization is a biological process that has important medical, economic and social implications. Our primary research interest is the mechanisms of sperm-egg interactions. This includes understanding the molecular events that mediate gamete recognition, adhesion, signaling and fusion. The genetic and molecular dissection of these events will also provide insights relevant to other important cell-cell interactions during the life and development of multicellular organisms.

Recent Publications

Krauchunas, AR, Marcello MR, Singson "A.  2016.  The molecular complexity of fertilization: Introducing the concept of a fertilization synapse. Molecular Reproduction and Development.
Singaravelu, G, Rahimi S, Krauchunas A, Rizvi A, Dharia S, Shakes D, Smith H, Golden A, Singson A.  2015.  Forward Genetics Identifies a Requirement for the Izumo-like Immunoglobulin Superfamily spe-45 Gene in Caenorhabditis elegans Fertilization.. Current Biology. 25:3220-3224.
Chatterjee, I, Ibanez-Ventoso C, Vijay P, Singaravelu G, Baldi C, Bair J, Ng S, Smolyanskaya A, Driscoll M, Singson A.  2013.  Dramatic fertility decline in aging C. elegans males is associated with mating execution deficits rather than diminished sperm quality. Exp. Gerontol.. 48:1156–1166. Abstract
Although much is known about female reproductive aging, fairly little is known about the causes of male reproductive senescence. We developed a method that facilitates culture maintenance of Caenorhabditis elegans adult males, which enabled us to measure male fertility as populations age, without profound loss of males from the growth plate. We find that the ability of males to sire progeny declines rapidly in the first half of adult lifespan and we examined potential factors that contribute towards reproductive success, including physical vigor, sperm quality, mating apparatus morphology, and mating ability. Of these, we find little evidence of general physical decline in males or changes in sperm number, morphology, or capacity for activation, at time points when reproductive senescence is markedly evident. Rather, it is the loss of efficient mating ability that correlates most strongly with reproductive senescence. Low insulin signaling can extend male ability to sire progeny later in life, although insulin impact on individual facets of mating behavior is complex. Overall, we suggest that combined modest deficits, predominantly affecting the complex mating behavior rather than sperm quality, sum up to block effective C. elegans male reproduction in middle adult life.