­­Homeodomain interacting protein kinase (HPK-1) is required in the soma for robust germline proliferation in <em>C. elegans</em> — ASN Events
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  2. Symposium 6B: Gene Regulation and Epigenetics
  3. ­­Homeodomain interacting protein kinase (HPK-1) is required in the soma for robust germline proliferation in C. elegans

­­Homeodomain interacting protein kinase (HPK-1) is required in the soma for robust germline proliferation in C. elegans (#99)

Slavica Berber 1 , Estelle LLamosas 2 , Priya Thaivalappil 1 , Peter R Boag 3 , Merlin Crossley 4 , Hannah R Nicholas 1
  1. School of Molecular Bioscience, University of Sydney, Sydney
  2. The Lowy Cancer Research Centre, University of NSW, Sydney
  3. Department of Biochemistry and Molecular Biology, Monash University, Melbourne
  4. School of Biotechnology and Biomolecular Sciences, University of NSW, Sydney

hpk-1 encodes the sole C. elegans member of a family of evolutionarily conserved protein kinases called the homeodomain interacting protein kinases (HIPKs). Mammalian homologues of HPK-1 have been implicated in control of numerous cellular processes including cell survival and proliferation. A C. elegans strain carrying a hpk-1 mutation has previously been studied (Raich et al., 2003), but no obvious phenotypes were reported. We decided to use the hpk-1 mutant strain and hpk-1 RNAi to investigate the role of HPK-1 in the development and maintenance of the C. elegans germline.

A significant reduction in germline proliferation was observed in the strain carrying the hpk-1 mutation. The phenotype was characterised by reduced brood size, reduced size of the mitotic region and a decrease in the number of proliferative cells. Knockdown of hpk-1 by RNAi resulted in a comparable phenotype, confirming that HPK-1 is required for normal germline proliferation. Our results furthermore suggest that HPK-1 is not only required for the maintenance of the mitotic region in adult germlines but that it is also necessary for the establishment of the progenitor pool during development as the reduced proliferation phenotype was also observed at the L4 stage.

Interestingly, the brood size and number of proliferative cells were rescued in hpk-1 mutants with HPK-1::mCherry-expressing transgenes from which no germline expression had been detected. In addition, knockdown of hpk-1 in a soma-sensitive RNAi strain resulted in reduced proliferative cell number whereas knockdown in a germline-sensitive RNAi strain had no significant effect. These observations suggest a role for HPK-1 in soma-dependent control of germline proliferation.