The authors, comprising researchers from Richard Poole’s lab, found evidence that key cell fate determinants have a previously unappreciated function in regulating unequal cleavage – and therefore cell size – of the parent cells whose daughter cell fates they then go on to specify. Their paper was featured as a Research Highlight and there was also a ‘People behind the papers’ interview (by email).
The development of multicellular organisms generates various cell types, each with its own unique molecular signature and specific cell size. Asymmetric cell division is one mechanism by which two daughter cells can acquire different fates. That asymmetric cell divisions can also generate daughters of unequal sizes has been known for over 100 years. However, why dividing cells regulate daughter cell size and whether this influences asymmetric fate specification remains unresolved.
This paper, published in the prestigious journal, Development, sheds light on this question. As one reviewer commented: “The authors propose the concomitant regulation of neural fate and cell size as a general mechanism to ensure adequate neuronal size during C. elegans embryonic development, where cell growth mechanisms do not operate”.
We also learn from the interview that, besides favouring the nematode worm,
C. elegans, as a model for such research – a move away from the zebrafish that Richard made whilst at Columbia University –Richard enjoys fishing in his spare time (see in the photo with a catch made on the Norfolk, UK coast). Lead author Thomas Mullan, on the other hand, has rather different interests, since he is busy learning not one but three languages during his commute to the lab: Latin, Japanese and Korean. When not doing that, Thomas – who originally joined Richard’s lab in the first year of his PhD – is motivated by an interest in the developmental origins and evolution of cell types and larger structures.
