ライフサイエンスコーパス: SASP

1 SASP components initiate and reinforce senescence in adj

2 SASP is a program that can be induced by oncogenes or DN

3 carcinogenesis by inducing senescence and a SASP.

4 However, some cells can develop a SASP comprising factors that are immunosuppressive and p

5 izing radiation or oncogenic RAS developed a SASP regardless of whether they expressed p16(INK4a).

6 vein endothelial cells (HUVECs) developed a SASP that could be suppressed by targeting the JAK pathw

7 NK4a)-positive cells may not always harbor a SASP in vivo and, furthermore, that the SASP is not a co

8 diated lipogenic state was found to induce a SASP in PMS iNSCs via cholesterol-dependent transcriptio

9 p21(CIP1/WAF1), induces senescence without a SASP, even though they induced other features of senesce

10 as(V12)-transformed NIH 3T3 cells, activated SASP gene expression, and recruited the CBP coactivator

11 etylase (HDAC) inhibitors robustly activated SASP in the absence of DNA breaks, suggesting that DDR-d

12 In addition, SASP-mediated endothelial cell activation stimulates the

13 form (P41) was assayed for activity against SASP and the zymogen form (P46) was assayed for the abil

14 Variants inactive against SASP and unable to autoprocess were analyzed by circular

15 8MAPK activation was sufficient to induce an SASP, and p53 restrained p38MAPK activation.

16 In SASP-A and SASP-C of Bacillus megaterium two conserved glutamate re

17 ated with a reduction in senescent cells and SASP, supporting a translational potential of targeting

18 , it remains uncertain which joint cells and SASP-factors contribute to the OA phenotype.

19 The structure of both DNA and SASP alters upon their association and this causes major

20 mation was associated with decreased OIS and SASP and a protumorigenic tumor microenvironment that ha

21 th colon cancer show high levels of PLD2 and SASP factor genes expression correlating with Wnt pathwa

22 diated cytoplasmic chromatin recognition and SASP during senescence.

23 s biliary constituents affect senescence and SASP in cultured human cholangiocytes.

24 nt reduction in cholangiocyte senescence and SASP is a new therapeutic approach for PSC.

25 anscription factor GATA4 as a senescence and SASP regulator.

26 e show that mice with reduced senescence and SASP responses exhibit decreased tumour-inducing potenti

27 ogated experimentally induced senescence and SASP.

28 sms involved in cholangiocyte senescence and SASP.

29 in bile induced cholangiocyte senescence and SASP.

30 d share a common signature of senescence and SASP.

31 , we consider the evidence for the SASP and "SASP-like" inflammation in driving skin carcinogenesis,

32 hese genes cause the loss of the appropriate SASP from spores, and the sspK, sspM and sspO (and likel

33 or tlp loci cause a loss of the appropriate SASP from spores, but have no discernible effect on spor

34 e that senescence and a stem cell-associated SASP drive cell transformation and tumour initiation in

35 Loss of HMGB2 during senescence blunts SASP gene expression by allowing for spreading of repres

36 s from a negative feedback loop activated by SASP-mediated endoplasmic reticulum (ER) stress.

37 We found that expression of the canonical SASP members interleukin (IL)-6 and IL-8, but not OPN, w

38 abase of soluble proteins and exosomal cargo SASP factors originating from multiple senescence induce

39 amined the molecular mechanisms that control SASP activation, focusing on the known SASP factor osteo

40 Here, we delineate another crucial SASP regulatory pathway and its relationship to the DDR

41 ely 1 h at 70 degrees C), and the deamidated SASP no longer bound to DNA effectively.

42 trategies that selectively block deleterious SASP components.

43 rotumorigenic property of the IL-1-dependent SASP in this context.

44 of DNA breaks, suggesting that DDR-dependent SASP activation occurs in response to chromatin remodeli

45 plication and DDR activation, thus disabling SASP expression.

46 scence-associated secretory phenotype (i.e., SASP).

47 n of the small, acid-soluble protein family (SASP) from spore samples on the MALDI sample holder.

48 ells, termed "senolytics" are a major focus, SASP-centered approaches are emerging as alternatives to

49 The removal of macroH2A1 from SASP genes results from a negative feedback loop activat

50 f ATM, which mediates removal macroH2A1 from SASP genes.

51 ation during OIS, including its removal from SASP gene chromatin.

52 consistent with the absence of a functional SASP.

53 The full activation of senescence genes (SASP genes and p53 targets) requires condensin; its depl

54 How SASP genes are excluded from SAHF-mediated global gene s

55 Additionally, we identify SASP senescence-associated secretory phenotype by using

56 In SASP-A and SASP-C of Bacillus megaterium two conserved g

57 ayed in spore outgrowth and more impaired in SASP degradation than were spores from a gpr single muta

58 eading us to investigate the role of MLL1 in SASP expression.

59 hese findings assign p38MAPK a novel role in SASP regulation--one that is necessary, sufficient, and

60 Chemotherapy-induced SASP could be limited by targeting the p38MAPK-MK2 pathw

61 spreading of repressive heterochromatin into SASP gene loci.

62 ntrol SASP activation, focusing on the known SASP factor osteopontin (OPN).

63 teins (SASP), but the DPA-less spores lacked SASP-gamma.

64 of the positive feedback loop that maintains SASP gene expression and triggers the induction of parac

65 racts from spores which lack the three major SASP (alpha, beta, and gamma).

66 Additionally, senescent melanocyte SASP induces telomere dysfunction in paracrine manner an

67 ition markedly reduced the secretion of most SASP factors, constitutive p38MAPK activation was suffic

68 pe, alpha/beta-type SASP but not by a mutant SASP that binds DNA poorly.

69 Notably, SASP sensitized breast cancer cells to inhibitors of the

70 r pro-inflammatory factors including a novel SASP component CLEC11A.

71 The specificity of the observed SASP peptides was evaluated using a cross-species sequen

72 c mice, as well as pharmacologic blockade of SASP, improved LCH disease in mice.

73 hromatin spreading to allow for exclusion of SASP gene loci from a global heterochromatin environment

74 lpha expression and restricted expression of SASP components IL-6 and IL-8.

75 This correlates with incorporation of SASP gene loci into SAHF.

76 GB2) orchestrates the chromatin landscape of SASP gene loci.

77 vel activity of simvastatin and mechanism of SASP regulation.

78 standing of both the roles and mechanisms of SASP expression may offer new targets for skin cancer pr

79 P and highlight the therapeutic potential of SASP modulation as complimentary or an alternative to cu

80 critical control point for the regulation of SASP gene expression during senescence.

81 scence and suppresses basal transcription of SASP genes.

82 however, these effects of MLL1 inhibition on SASP gene expression do not impair OIS and, furthermore,

83 enescence-associated secretory phenotype, or SASP), and reduced expression of the nuclear lamina prot

84 s a novel master regulator that orchestrates SASP through prevention of heterochromatin spreading to

85 a senescence-associated secretory phenotype (SASP) able to increase the stem properties of cancer cel

86 e senescence-associated secretory phenotype (SASP) and IL-6 expression.

87 a senescence-associated secretory phenotype (SASP) characterized by IL1B, CXCL8, CCL2, TNF, CCL27 and

88 d senescence-associated secretory phenotype (SASP) components.

89 s senescence-associated secretory phenotype (SASP) contribute to chemotherapy-induced bone loss that

90 , p19ARF, and DcR2) and secretory phenotype (SASP) factors (PAI-1 and IL6).

91 d senescence-associated secretory phenotype (SASP) gene expression profile.

92 e senescence-associated secretory phenotype (SASP) gene transcription signature.

93 f senescence-associated secretory phenotype (SASP) genes whose induction by oncogenic stress requires

94 e senescence-associated secretory phenotype (SASP) has been implicated in cartilage degradation and O

95 e senescence-associated secretory phenotype (SASP) has recently emerged as a driver of and promising

96 d senescence-associated secretory phenotype (SASP) in livers of patients with PSC, primary biliary ci

97 n senescence-associated secretory phenotype (SASP) in particular have revealed various layers of func

98 e senescence-associated secretory phenotype (SASP) in systemic aging, sirtuin family regulation of me

99 s senescence-associated secretory phenotype (SASP) includes various factors that are synthesized as t

100 a senescence-associated secretory phenotype (SASP) involving the production of factors that reinforce

101 e senescence-associated secretory phenotype (SASP) is a hallmark of senescence with an important phys

102 e senescence-associated secretory phenotype (SASP) of IVD cells.

103 e senescence-associated secretory phenotype (SASP) of senescent tumor cells through activation of mat

104 e senescence-associated secretory phenotype (SASP) specifically in visceral adipose tissue.

105 e senescence-associated secretory phenotype (SASP) that attenuates acinar-to-ductal metaplasia, pancr

106 a senescence-associated secretory phenotype (SASP) that coincided with the development of tubulointer

107 e senescence-associated secretory phenotype (SASP) that contribute to tumor suppression by enforcing

108 a senescence-associated secretory phenotype (SASP) that includes pro-angiogenic factors that promote

109 a senescence-associated secretory phenotype (SASP) that turns senescent fibroblasts into proinflammat

110 y senescence-associated secretory phenotype (SASP) through recognizing cytoplasmic chromatin during s

111 a senescence-associated secretory phenotype (SASP) with influx of proinflammatory macrophages, ultima

112 e senescence-associated secretory phenotype (SASP), a pro-inflammatory response linked to tumor promo

113 he senescent-associated secretory phenotype (SASP), and over expression of H2A.J increases the expres

114 s senescence-associated secretory phenotype (SASP), dominated by IL-6.

115 a senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, and alterations in DNA

116 e senescence-associated secretory phenotype (SASP), senescent cells can paradoxically promote carcino

117 a senescence-associated secretory phenotype (SASP), the function of which is unclear.

118 a senescence-associated secretory phenotype (SASP), whether these cells are capable of initiating tum

119 e senescence-associated secretory phenotype (SASP), which can reinforce the arrest and induce senesce

120 e senescence-associated secretory phenotype (SASP), which has been postulated to carry both pro- and

121 e senescence-associated secretory phenotype (SASP), which helps to maintain the senescent state and t

122 e senescence-associated secretory phenotype (SASP), which is correlated with cancer cell proliferatio

123 e senescence-associated secretory phenotype (SASP), which itself favors reprogramming.

124 , senescence-associated secretory phenotype (SASP)-mediated tissue damage, and involvement in adipose

125 e senescence-associated secretory phenotype (SASP).

126 e senescence-associated secretory phenotype (SASP).

127 e senescence-associated secretory phenotype (SASP).

128 e senescence-associated secretory phenotype (SASP).

129 e senescence-associated secretory phenotype (SASP).

130 y senescence-associated secretory phenotype (SASP).

131 e senescence-associated secretory phenotype (SASP).

132 e senescence-associated secretory phenotype (SASP).

133 eam regulator of the SA secretory phenotype (SASP).

134 a senescence-associated secretory phenotype (SASP).

135 e senescence-associated secretory phenotype (SASP).

136 e senescence-associated secretory phenotype (SASP).

137 e senescence-associated secretory phenotype (SASP).

138 a senescence-associated secretory phenotype (SASP).

139 d senescence-associated secretory phenotype (SASP).

140 factors involved in SA-secretory phenotype (SASP).

141 e senescence-associated secretory phenotype (SASP).

142 e senescence-associated secretory phenotype (SASP).

143 e senescence-associated secretory phenotype (SASP).

144 e senescence-associated secretory phenotype (SASP).

145 e senescence-associated secretory phenotype (SASP).

146 e senescence-associated secretory phenotype (SASP).

147 -based interventions to inhibit the proaging SASP.

148 nditions; expression of profibroinflammatory SASP components (i.e., IL-6, IL-8, CCL2, PAI-1) was also

149 e a senescence-associated secretory profile (SASP) that is rich in CXCR2 ligands, which drive fibrobl

150 signalling axis promotes the proinflammatory SASP by enhancing glycolysis and mitochondrial respirati

151 salvage pathway, governs the proinflammatory SASP independent of senescence-associated growth arrest.

152 oteins and NAMPT promote the proinflammatory SASP through NAD(+)-mediated suppression of AMPK kinase,

153 our-promoting effects of the proinflammatory SASP, our results suggest that anti-ageing dietary NAD(+

154 AD(+) metabolism governs the proinflammatory SASP.

155 eta-type, small, acid-soluble spore protein (SASP) from Bacillus subtilis, was generated that has a v

156 beta-type small, acid-soluble spore protein (SASP) of Bacillus subtilis took place readily in vitro (

157 beta-type small, acid-soluble spore protein (SASP) SspC(wt) were designed to evaluate the contributio

158 protease's small acid-soluble spore protein (SASP) substrates, SASP-gamma.

159 ith a group of small, acid-soluble proteins (SASP) that protect DNA from a variety of harsh treatment

160 encoding minor small, acid-soluble proteins (SASP) unique to spores of Bacillus subtilis are expresse

161 ing new, minor small, acid-soluble proteins (SASP) unique to spores of Bacillus subtilis are expresse

162 Eleven small, acid-soluble proteins (SASP) which are present in spores but not in growing cel

163 lpha/beta-type small, acid-soluble proteins (SASP), colocalized to these nucleoid rings early in spor

164 lpha/beta-type small, acid-soluble proteins (SASP), that protect the spore's DNA against different ty

165 lpha/beta-type, small acid-soluble proteins (SASP), which are the major chromosomal proteins in spore

166 e core known as small acid-soluble proteins (SASP).

167 lpha/beta-type small, acid-soluble proteins (SASP).

168 eta-type small, acid-soluble spore proteins (SASP) are essential for the resistance of DNA in spores

169 mma-Type small, acid-soluble spore proteins (SASP) are the most abundant proteins in spores of at lea

170 ation of small, acid-soluble spore proteins (SASP) during germination of spores of Bacillus and Clost

171 beta-type small acid-soluble spore proteins (SASP) is the major determinant of DNA resistance to dama

172 eta-type small, acid-soluble spore proteins (SASP) of Bacillus species were readily oxidized to methi

173 Small, acid-soluble spore proteins (SASP) of the alpha/beta-type from several Bacillus speci

174 eta-type small, acid-soluble spore proteins (SASP) that are synthesized in the developing forespore a

175 eta-type small, acid-soluble spore proteins (SASP) to DNA of spores of Bacillus species is the major

176 beta-type small acid-soluble spore proteins (SASP), but the DPA-less spores lacked SASP-gamma.

177 group of small, acid-soluble spore proteins (SASP), which are synthesized in the developing spore and

178 More broadly, MLL1 inhibition also reduces "SASP-like" inflammatory gene expression from cancer cell

179 cid-soluble spore protein (SASP) substrates, SASP-gamma.

180 h the pharmacologic inhibitor sulfasalazine (SASP).

181 We speculate that SASP inhibition by JAK inhibitors may contribute to alle

182 The SASP is proposed to underlie age-related pathologies, in

183 what tumor stage and how senescence and the SASP act on endogenous tumor growth in vivo is unknown.

184 omas, and low expression of both RB1 and the SASP genes was associated with poor prognosis.

185 hondrial function, and suppress CCFs and the SASP in senescent cells.

186 Therefore, senescent cells and the SASP represent significant opportunities for advancement

187 ible contribution of senescent cells and the SASP to age-related inflammation and frailty.

188 s based on targeting senescent cells and the SASP, and potential paths to developing clinical interve

189 he mechanisms that induce senescence and the SASP, their associations with chronic disease and frailt

190 indicate a potential association between the SASP and cGVHD development in LGs and suggest that targe

191 a DNA binding protein and is cleaved by the SASP-specific protease (GPR) at a site similar to that c

192 Here, we show that simvastatin decreases the SASP of senescent human fibroblasts by inhibiting protei

193 his review, we consider the evidence for the SASP and "SASP-like" inflammation in driving skin carcin

194 covers a primary and beneficial role for the SASP in promoting cell plasticity and tissue regeneratio

195 se findings define a beneficial role for the SASP in tissue repair and help to explain why the SASP e

196 a complex and often conflicting role for the SASP in tumorigenesis and treatment response.

197 ng is essential, but not sufficient, for the SASP, which is restrained by p53.

198 ndergoing senescence and is required for the SASP.

199 hway that drives CCF formation and hence the SASP.

200 However, the SASP has also been shown to favor embryonic development,

201 In the SASP of cells that became senescent following several in

202 Mechanistically, p38MAPK induced the SASP largely by increasing NF-kappaB transcriptional act

203 anscription factor NF-kappaB to initiate the SASP and facilitate senescence.

204 Likewise, the SASP in treated cancers can either contribute to durable

205 ummarize the regulation and functions of the SASP and highlight the therapeutic potential of SASP mod

206 pression closely correlated with that of the SASP cassette in human osteosarcomas, and low expression

207 activation promotes OIS via elevation of the SASP factor CXCL1 (also known as KC), which activates CX

208 primary oocytes and the transcription of the SASP factors in the ovary, in addition, led to increased

209 Here we uncover timely new functions of the SASP in promoting a proregenerative response through the

210 tory phenotype through the regulation of the SASP initiator IL-1alpha, creating a microenvironment pe

211 However, the in vivo effect of the SASP is poorly understood due to the difficulty of study

212 and, furthermore, abolish the ability of the SASP to enhance cancer cell proliferation.

213 Despite the importance of the SASP to tumor biology, it is virtually unknown how trans

214 of senescent cells and the expression of the SASP while nullifying the damaging effects of the FFD on

215 that inhibiting the major components of the SASP, including IL-6 and CXCL9, with senolytics is a pot

216 NF-kappaB acts as a master regulator of the SASP, influencing the expression of more genes than RB a

217 The complexity of the SASP, typically assessed by a few dozen secreted protein

218 ss is known about pathways that regulate the SASP.

219 Further, p38MAPK regulated the SASP independently of the canonical DDR.

220 role of NAD(+) metabolism in regulating the SASP is poorly understood.

221 rstood due to the difficulty of studying the SASP independently of other senescence-associated phenot

222 irect role for p16(INK4a) in suppressing the SASP.

223 or a SASP in vivo and, furthermore, that the SASP is not a consequence of p16(INK4a) activation or se

224 However, prolonged exposure to the SASP causes a subsequent cell-intrinsic senescence arres

225 use keratinocytes transiently exposed to the SASP exhibit increased expression of stem cell markers a

226 mary alveolar bone cells were exposed to the SASP via in vitro senescent conditioned media (SCM) admi

227 the nucleus of senescent cells, trigger the SASP through activation of the innate immunity cytosolic

228 in-1 (IL-1) pathway completely uncouples the SASP from other senescence-associated phenotypes such as

229 1beta signal through IL-1R to upregulate the SASP in a cooperative manner.

230 AML blast survival and proliferation via the SASP.

231 in tissue repair and help to explain why the SASP evolved.

232 Here, we present the "SASP Atlas," a comprehensive proteomic database of solub

233 effective chemo- and immunotherapies through SASP-dependent effects on the tumor vasculature and immu

234 related pathologies and inflammation through SASP secretion.

235 ifespan in vivo, potentially in part through SASP reduction.

236 g endospore-forming bacteria, contributes to SASP degradation but that its function is normally maske

237 HMGB2 preferentially localizes to SASP gene loci during senescence.

238 escribe how chromatin-bound HMGB2 fine tunes SASP expression by avoiding heterochromatin spreading.

239 es lacking one or both major alpha/beta-type SASP (alpha- and alpha- beta- strains, respectively).

240 s or in spores lacking major alpha/beta-type SASP (alpha- beta- spores) had no effect on sporulation

241 genome, including two minor alpha/beta-type SASP (SspC and SspD) and a putative spore coat protein (

242 wo methionine residues of an alpha/beta-type SASP (SspC) in spores of Bacillus subtilis, although one

243 In the complex, the alpha/beta-type SASP adopt a helix-turn-helix motif, interact with DNA t

244 y, but DNA binding protected alpha/beta-type SASP against methionine oxidation by peroxides in vitro.

245 ubtilis spores lacking major alpha/beta-type SASP and overexpressing SspC(DeltaN11-D13K-C3) had a 10-

246 of the spores' pool of major alpha/beta-type SASP and was delayed when alpha/beta-type SASP degradati

247 However, alpha/beta-type SASP are even more strongly protected against deamidatio

248 re at 2.1 A resolution of an alpha/beta-type SASP bound to a 10-bp DNA duplex.

249 of either of two wild-type, alpha/beta-type SASP but not by a mutant SASP that binds DNA poorly.

250 y be important in vivo since alpha/beta-type SASP containing oxidized methionine residues no longer b

251 here it is bound to DNA, the alpha/beta-type SASP deamidated with a t(1/2) of 2 to 3 h at 95 degrees

252 omplex and the physiology of alpha/beta-type SASP degradation during spore germination are discussed.

253 pe SASP and was delayed when alpha/beta-type SASP degradation was delayed.

254 ts rapid degradation of this alpha/beta-type SASP early in germination.

255 In all four alpha/beta-type SASP examined, the amino donor in the EDC induced amide

256 P, variants of SspC (a minor alpha/beta-type SASP from Bacillus subtilis) with modified N termini wer

257 te the interchangeability of alpha/beta-type SASP in DNA protection in spores.

258 ing with oxidative damage to alpha/beta-type SASP in spores is DNA binding, which protects the protei

259 synthesize both DPA and most alpha/beta-type SASP in strain PS3664 (sspA sspB sleB spoVF) resulted in

260 A mutant alpha/beta-type SASP in which the reactive asparagine was changed to asp

261 Folding of alpha/beta-type SASP induced by a variety of DNAs and oligonucleotides w

262 The primary sequence of alpha/beta-type SASP is highly conserved; however, the N-terminal third

263 These results indicate that alpha/beta-type SASP may well have global effects on gene expression dur

264 These oxidized alpha/beta-type SASP no longer bound to DNA effectively, but DNA binding

265 pores, HBsu colocalized with alpha/beta-type SASP on the nucleoid, suggesting that HBsu could modulat

266 in modulating the effects of alpha/beta-type SASP on the properties of DNA in the developing and dorm

267 Thus, not only do alpha/beta-type SASP protect spore DNA from damage; DNA also protects al

268 ular details of both DNA and alpha/beta-type SASP protection in the complex and thus also in spores.

269 ies showed that HBsu altered alpha/beta-type SASP protection of pUC19 from DNase digestion, induced n

270 of a model for DNA-dependent alpha/beta-type SASP protein-protein interaction involving the N-termina

271 Analysis of several alpha/beta-type SASP showed that these proteins have essentially no seco

272 moderately strong binding of alpha/beta-type SASP to DNA is important to balance the potentially conf

273 However, the alpha/beta-type SASP was extremely resistant to deamidation within spore

274 which is highly conserved in alpha/beta-type SASP was only oxidized to a small degree.

275 h several of the DNA-binding alpha/beta-type SASP were present.

276 Incubation of an oxidized alpha/beta-type SASP with peptidyl methionine sulfoxide reductase (MsrA)

277 to methionine, restored the alpha/beta-type SASP's ability to bind to DNA.

278 resistance on spores lacking alpha/beta-type SASP, and spores with SspC(Delta11-D13K) triggered germi

279 ndicate that, in addition to alpha/beta-type SASP, DPA also is extremely important in spore resistanc

280 An alpha/beta-type SASP, Ssp2, from Clostridium perfringens was expressed a

281 is of the interaction of one alpha/beta-type SASP, SspC(Tyr), with DNA indicated that each binding ev

282 ifferences between different alpha/beta-type SASP, the N-terminal regions of these proteins are invol

283 in the N-terminal region of alpha/beta-type SASP, variants of SspC (a minor alpha/beta-type SASP fro

284 no longer bind DNA well and alpha/beta-type SASP-DNA binding is essential for long-term spore surviv

285 vity factors (omega), as the alpha/beta-type SASP-DNA interaction was significantly cooperative, with

286 um binding parameters of the alpha/beta-type SASP-DNA interaction.

287 ificantly interfere with the alpha/beta-type SASP-mediated changes in the UV photochemistry of DNA th

288 and greatly ameliorated the alpha/beta-type SASP-mediated increase in DNA persistence length.

289 ve DNA supercoiling opposing alpha/beta-type SASP-mediated positive supercoiling, and greatly amelior

290 ing that HBsu could modulate alpha/beta-type SASP-mediated properties of spore DNA.

291 spores with lower levels of alpha/beta-type SASP.

292 ynthesis of normal levels of alpha/beta-type SASP.

293 om damage; DNA also protects alpha/beta-type SASP.

294 acking the majority of their alpha/beta-type SASP.

295 e similar to that cleaved in alpha/beta-type SASP.

296 ngs for the structure of the alpha/beta-type SASP.DNA complex and the physiology of alpha/beta-type S

297 A gamma-type SASP of B. subtilis also deamidated readily in vitro (t(

298 Current work has shown that the gamma-type SASP or their coding genes (sspE genes) are present in m

299 In addition, no gamma-type SASP were found in A. acidocaldarius spores, although se

300 termining the precise function of gamma-type SASP.