PDF(Pubmed)
Abstract：
Mammalian cardiomyocytes (CMs) mostly become polyploid shortly after birth. Because this feature may relate to several aspects of heart biology, including regeneration after injury, the mechanisms that cause polyploidy are of interest. BALB/cJ and BALB/cByJ mice are highly related sister strains that diverge substantially in CM ploidy. We identified a large deletion in the Cyth1 gene that arose uniquely in BALB/cByJ mice that creates a null allele. The deletion also results in ectopic transcription of the downstream gene Dnah17, although this transcript is unlikely to encode a protein. By evaluating the natural null allele from BALB/cByJ and an engineered knockout allele in the C57BL/6J background, we determined that absence of Cyth1 does not by itself influence CM ploidy. The ready availability of BALB/cByJ mice may be helpful to other investigations of Cyth1 in other biological processes.
摘要：
哺乳动物心肌细胞(CMs)大多在出生后不久变成多倍体。因为这个特征可能与心脏生物学的几个方面有关，包括损伤后的再生,引起多倍体的机制是令人感兴趣的。BALB/cJ和BALB/cByJ小鼠是高度相关的姐妹品系，在CM倍性上大不相同。我们确定了Cyth1基因中的大缺失，该缺失在BALB/cByJ小鼠中独特地出现，产生了无效等位基因。该缺失还导致下游基因Dnah17的异位转录,尽管该转录物不太可能编码蛋白质。通过评估来自BALB/cByJ的天然无效等位基因和C57BL/6J背景中的工程化敲除等位基因，我们确定Cyth1的缺失本身不会影响CM倍性。BALB/cByJ小鼠的现成可用性可能有助于Cyth1在其他生物学过程中的其他研究。
