Muhlrad Paul J, Ward Samuel
Department of Molecular and Cellular Biology, The University of Arizona, Tucson, Arizona 85721, USA.
Genetics. 2002 May;161(1):143-55. doi: 10.1093/genetics/161.1.143.
Immature spermatids from Caenorhabditis elegans are stimulated by an external activation signal to reorganize their membranes and cytoskeleton to form crawling spermatozoa. This rapid maturation, termed spermiogenesis, occurs without any new gene expression. To better understand this signal transduction pathway, we isolated suppressors of a mutation in the spe-27 gene, which is part of the pathway. The suppressors bypass the requirement for spe-27, as well as three other genes that act in this pathway, spe-8, spe-12, and spe-29. Eighteen of the suppressor mutations are new alleles of spe-6, a previously identified gene required for an early stage of spermatogenesis. The original spe-6 mutations are loss-of-function alleles that prevent major sperm protein (MSP) assembly in the fibrous bodies of spermatocytes and arrest development in meiosis. We have isolated the spe-6 gene and find that it encodes a predicted protein-serine/threonine kinase in the casein kinase 1 family. The suppressor mutations appear to be reduction-of-function alleles. We propose a model whereby SPE-6, in addition to its early role in spermatocyte development, inhibits spermiogenesis until the activation signal is received. The activation signal is transduced through SPE-8, SPE-12, SPE-27, and SPE-29 to relieve SPE-6 repression, thus triggering the formation of crawling spermatozoa.
秀丽隐杆线虫的未成熟精子细胞会受到外部激活信号的刺激,从而重组其细胞膜和细胞骨架,形成可游动的精子。这种快速成熟过程,即精子形成,在没有任何新基因表达的情况下发生。为了更好地理解这一信号转导途径,我们分离出了spe-27基因(该途径的一部分)突变的抑制子。这些抑制子绕过了对spe-27以及该途径中其他三个基因spe-8、spe-12和spe-29的需求。18个抑制子突变是spe-6的新等位基因,spe-6是先前确定的精子发生早期所需的基因。最初的spe-6突变是功能丧失型等位基因,可阻止精子细胞纤维体中主要精子蛋白(MSP)的组装,并使减数分裂中的发育停滞。我们已经分离出spe-6基因,发现它编码一种酪蛋白激酶1家族中预测的蛋白丝氨酸/苏氨酸激酶。抑制子突变似乎是功能减弱型等位基因。我们提出了一个模型,据此SPE-6除了在精子细胞发育中起早期作用外,还会抑制精子形成,直到接收到激活信号。激活信号通过SPE-8、SPE-12、SPE-27和SPE-29进行转导,以解除SPE-6的抑制作用,从而触发可游动精子的形成。