KCH kinesin drives nuclear transport and cytoskeletal coalescence for tip cell growth

Abstract

Long-distance transport along microtubules (MTs) is critical for intracellular organisation. In animals, antagonistic motor proteins kinesin (plus end-directed) and dynein (minus end-directed) drive cargo transport. In land plants, however, the identity of motors responsible for transport is poorly understood, as genes encoding cytoplasmic dynein are missing. How other functions of dynein are brought about in plants also remains unknown. Here, we show that a subclass of the kinesin-14 family, KCH--which can also bind actin--drives MT minus end-directed nuclear transport in the moss Physcomitrella patens. When all four KCH genes were deleted, the nucleus was not maintained in the cell centre but was translocated to the apical end of protonemal cells. In the knockout (KO) line, apical cell tip growth was also severely suppressed. KCH was localised on MTs, including at the MT focal point near the tip where MT plus ends coalesced with actin filaments. MT focus was not persistent in KCH KO lines, whereas actin destabilisation also disrupted the focus despite KCH remaining on unfocused MTs. Functions of nuclear transport and tip growth were distinct, as a truncated KCH construct restored nuclear transport activity but not tip growth retardation of the KO line. Thus, our study identified KCH as a long-distance retrograde transporter as well as a cytoskeletal crosslinker, reminiscent of the versatile animal dynein.